Journal of ISSN: 2374-6947JDMDC

Diabetes, Metabolic Disorders & Control
Review Article
Volume 3 Issue 1 - 2016
Vitamin D Deficiency is a Surrogate Marker for Visceral Fat Content, Metabolic Syndrome, Type 2 Diabetes, and Future Metabolic Complications
Sunil J Wimalawansa*
Department of Medicine, Cardo Metabolic Institute, USA
Received: January 15, 2016 | Published: February 23, 2016
*Corresponding author: Sunil J Wimalawansa, Department of Medicine, Cardo Metabolic Institute, USA, Email:
Citation: Wimalawansa SJ (2016) Vitamin D Deficiency is a Surrogate Marker for Visceral Fat Content, Metabolic Syndrome, Type 2 Diabetes, and Future Metabolic Complications. J Diabetes Metab Disord Control 3(1): 00059. DOI: 10.15406/jdmdc.2016.03.00059


Worldwide, epidemics of obesity, type 2 diabetes (T2D), metabolic syndrome, and vitamin D deficiency have emerged during the past three decades. These are in part due to changing of behavior and; poverty and the increased consumption of poor-quality, caloric-dense, cheap food; sedentary lifestyles; and less exposure to sunlight. Thus, these four diseases have some common origins. This article highlights the importance of serum vitamin D levels, the common link, in diagnosis and management of these four common disorders. Making a right diagnosis early would allow targeted, cost-effective interventions to reverse abnormalities and prevent the development of major complications that require expensive interventions later. Two such distinctive markers that need to be identified are visceral obesity and vitamin D deficiency. Such identification can be achieved simply by measuring standardized abdominal girth using a tape measure and serum 25 hydroxy vitamin D levels. These two surrogate markers are inversely correlated but not mutually exclusive. Thus, they can be used as clinically useful practical guidance, not only for screening but also for follow-up progress and effective management of the aforementioned disorders. The combination of having a higher waist circumference and lower serum 25 hydroxy vitamin D levels is an effective clinical tool for identifying those who are at a higher risk for the development of future metabolic complications.

Keywords: 25-hydroxyvitamin D; Cardiovascular disease; Lipids; Premature mortality; Vitamin D insufficiency; Obesity


CDC: Centers for Disease Control and Prevention; BMI: Body Mass Index; CVD: cardiovascular disease; NAFLD: Non-Alcoholic Fatty Liver Disease; HDL: High Density Lipoproteins; LDL: Low Density Lipoproteins


Worldwide, more than 1 billion people have vitamin D insufficiency [1,2] and an additional 750 million have vitamin D deficiency [3,4]. However, the reported prevalence of vitamin D deficiency varies from 10% to 70% in different countries [4-6]. Because vitamin D deficiency is associated with multiple disorders, it has gained attention as a major public health problem [4]. However, it is key nutritional deficiency that is easily and cost-effectively treated [6-8].

The epidemics of obesity and type 2 diabetes (T2D) manifest in recent years result in part from excessive consumption of calories (mostly through calorie-dense fast food and fructose/corn syrup-based products and sugary drinks) in the presence of inadequate physical activities, the inappropriate and overuse of broad-spectrum antibiotics, chronic inflammation, infections, and diseases associated with poverty/low living standards [9-16].

According to the Centers for Disease Control and Prevention (CDC), more than one-third of adults (34.9%) and 17% of youth in the United States are obese [17,18]. The estimated annual medical cost related to obesity in the Unites States in 2012 was $190.2 billion; which is nearly 21% of the nation’s annual medical spending. The estimated annual medical costs for obese people were one-third higher than those who were of normal weight [19,20], but the associated stigma discourages people from seeking treatment [21].

Although obesity affects more than 600 million people in the world, another 350 million have undiagnosed obesity, particularly those with relatively normal body mass index (BMI) but who have intra-abdominal (i.e., visceral) obesity. Obesity is a global, preventable health problem of epidemic proportions and a major risk factor for chronic diseases, resulting in accelerated morbidity and premature mortality.

Obesity contributes to a host of non-communicable diseases, including cardiovascular disease (CVD), strokes, sleep apnea, depression, psycho-social problems, non-alcoholic fatty liver disease (NAFLD), inflammatory bowel disease (IBD), chronic kidney disease, increased risk for cancer, and osteoarthritis, and often leads to losses in productivity [12,13,16,22-25].

In the United States, about one-third of adults are obese and another third overweight [20,26-29]. Many persons with overweight or obesity have dyslipidemia, associated with raised serum levels of small density-low density lipoproteins (LDL), functionally impaired high density lipoproteins (HDL), and increased remnant particles secondary to reduced clearance of triglyceride-rich lipoproteins (raised triglycerides), which significantly increase CVD risks and events in persons with obesity [16,30]. Despite the availability of various pharmaceutical agents, lifestyle modification is the principal approach to preventing weight gain and reducing obesity-related CVD and other risks [27,28,31,32].

Measurement of visceral fat

Estimating visceral fat is important not only to identify individuals who are at higher risk for future CVD complications [33,34] but also as a tool to identify those who are deficient in vitamin D. Anthropometric indices such as abdominal girth [waist circumference (WC)] and BMI have been used to categorize overweightness and obesity and explore relationships between obesity and vitamin D [2,34-41]. However, the inability to distinguish visceral fat using the BMI precludes its usefulness for assessing abdominal fat contents or determining a therapeutic course in many ethnic groups.

The accuracy of identifying the visceral fat contents can be improved with newer techniques, such as bioelectrical impedance analysis, dual-energy x-ray absorptiometry, computed tomography, and magnetic resonance imaging [42-46]. Nevertheless, these technologies are expensive, have associated radiation hazards, and are not cost-effective tools for screening the general population to identify and quantify visceral fat content in a clinically meaningful manner [47,48]. Having higher WC and lower serum 25(OH)D levels is a better combined tool for identifying those who are at higher risk for future metabolic complications than is WC alone, WC plus lipid profiles, or expensive imaging techniques.

Obesity-Importance of reducing visceral fat content

Obesity is a disease with major public health, social, and economic consequences that require serious attention from all stakeholders. Obesity is much more complicated than being just a lifestyle issue. In addition to the caloric imbalances, those who are genetically prone to accumulate weight have abnormalities of the mitochondria, which play central roles in energy expenditure and energy balance, and have genetic predispositions [39].

Like other diseases, obesity has

  1. a cause (caloric imbalance, availability and abundance of food, and consumption of low-nutritious, high-caloric food);
  2. Pathology (adipocyte-mediated excessive production of inflammatory cytokines and hormones);
  3. pathophysiology (an environmentally and psychologically inducible dysregulation of appetite, low activity levels, body fat distribution, psychological issues, and deranged body-weight–controlling mechanisms) [49], and
  4. Is a disease that can be treated (with anti-obesity medication) [31,38].

Although there are common causes, each individual has a different set of risk factors that lead to the development of overweight and obesity. Moreover, if the excess weight issue is untreated, many of those with obesity end up with serious complications [50-52]. An effective strategy necessitates preventing individuals from becoming overweight and requires identification of the cause(s) of obesity in individual persons. Clinicians should have the ability to provide individualized care and treatment plans for their patients to assist them in losing weight and reducing complications.

Intra-abdominal (visceral) fat is a key site for generating inflammatory cytokines that lead to various metabolic abnormalities in the presence of obesity. This leads to a vicious cycle of systemic inflammation [53,54]. Therefore, reducing intra-abdominal fat (using waist size is a surrogate marker) is a prime target in reducing insulin resistance and preventing future complications.

Decreasing the visceral fat burden is associated with improvements in most of the treatable abnormalities of metabolic syndrome, including hypertension, dyslipidemia, chronic inflammation, and development of T2D. Such approaches would not only minimize future serious metabolic complications but also improve quality of life and engender cost savings in the long run.

Visceral obesity and T2D

The prevalence of visceral obesity, T2D, and vitamin D deficiency increases with age. Increasing abdominal girth (measured as waist circumference) is a reasonable surrogate marker for abdominal obesity and excess visceral fat. Visceral adiposity is associated with CVD, metabolic syndrome, and T2D, particularly in ethnic minorities and Asians [38,55-57]. Successful treatment in reducing visceral adiposity leads to reduction of the risk of T2D [58,59].

In addition to deranged handling of glucose and free fatty acids, diabetes has an underlying generalized, chronic inflammatory status [60-62]. Patients with T2D and chronic kidney disease have impaired endothelial function and vitamin D, and its analogs may play a role in regulation of endothelial function and inflammation [63]. Insulin resistance, obesity, and T2D are associated with a marked increase in atherosclerosis coronary heart disease and stroke [64].

Those with insulin resistance, obesity, and/or T2D have chronically elevated inflammatory markers, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), further supporting the underlying inflammation and oxidative stress. A similar etiology is existing with the chronic, hyper-caloric-malnutrition (obesity). These are thought to interfere with the anti-inflammatory effect of insulin, which in turn might promote inflammation [65]. Because vitamin D has anti-inflammatory effects [66-70], it is not surprising that it has effects on improving blood sugar control, islet cell functions, insulin release, and decreasing insulin resistance [4,64,65].

Visceral fat and metabolic syndrome

Metabolic studies have demonstrated that among equally obese patients, subjects with excess visceral adipose tissue have the metabolic profile with the highest risks [71,72]. Accumulation of visceral adiposity precedes the development of type 2 diabetes in most ethnic groups [31]. This is highlighted in a clinical study in Japanese Americans, which demonstrated an effect independent of fasting insulin, insulin secretion, glycaemia, total and regional adiposity, and family history of diabetes as a cause and a predictor for genesis of T2D [73,74].

The correlation of abdominal adiposity has been reported with various components of metabolic syndrome, including anthropometric parameters and insulin resistance [55-57,75]. Visceral fat is an organ that releases large number of harmful chemicals (cytokines) that lead to chronic inflammation, which particularly affects the liver and vascular system [4,6]. Chemicals generated by hypertrophic visceral fat cells and macrophages reach the liver directly via the portal venous system, thus exposing it to a high contents of inflammatory agents that impair its functions, including derangement of glucose and fatty acid metabolism.

Rectification of vitamin D deficiency decreases insulin resistance

Several observational studies have demonstrated a consistent association of low serum 25(OH)D levels with diabetes, pre-diabetes, obesity, and metabolic syndrome [76,77]. A population-based study from Norway confirmed a strong inverse association between elevated BMI and low serum 25(OH)D levels [78]. In addition, the serum level of 25(OH)D is inversely correlated with the average blood sugar concentrations and insulin resistance [79].

In patients with T2D, vitamin D supplementation increases insulin sensitivity, releases insulin, and decreases diabetes-associated chronic inflammation [80]. Vitamin D stimulates insulin production in the pancreas and may play a role in preventing type 2 diabetes through its ability to decrease inflammation, insulin resistance, insulin synthesis and secretion [81], and perhaps decreased inflammation [69,70]. Moreover, vitamin D and calcium intake are inversely associated with the risk of T2D [82]. Those who consume three or more servings of vitamin D-fortified dairy products a day are at a lower risk for diabetes [83].

Vitamin D also plays a role in insulin signaling [84] and modifying the risks of diabetes [85-87]. The findings of vitamin D receptors in pancreatic b cells [88,89] further supports the notion that vitamin D influences insulin synthesis and secretion. Deficiency of vitamin D predisposes individuals to type 1 and type 2 diabetes and perhaps inadequate responses to anti-diabetes therapies [89-93].

Inverse correlations of decreasing levels of serum 25(OH)vitamin D [25(OH)D] levels with the prevalence of type 2 diabetes (T2D) and metabolic syndrome (MS); the latter has the most predominant relationship. Negative correlations of 25(OH)D are higher with the waste circumference (WC; abdominal girth) in comparison to the body mass index (BMI). Direct or indirect associations of varying levels of serum 25(OH)D with four indices are presented in the figure. Graphic presentations are based on best estimates and construct on hypothetical basis (thus only in approximation). Broken green line represent the changing serum 25(OH) D levels (Figure 1).

Figure 1: Estimated relationships between serum 25 (OH) vitamin D levels with WC and BMI, and T2D and metabolic syndrome.

Physiological functions of vitamin D

The traditional benefits of vitamin D are well recognized in the musculoskeletal system, including maintenance of calcium homoeostasis and bone mineralization [3,4,6,94,95]. Vitamin D enhances intestinal calcium absorption and mineralization of osteoid tissues, thus increasing bone strength [7,96-98]. Rickets in children and osteomalacia in adults are classic manifestations of severe vitamin D deficiency [4,97]. Vitamin D also decreases the incidence of falls and thus fractures [4,97,99]. Extra skeletal functional benefits of vitamin D in various non-communicable diseases and infection control also have been reported [2,6,9].

Epidemiologic and cohort studies suggest that low 25 hydroxy vitamin D [25(OH)D] affects numerous and diverse physiologic functions, such as control of cell growth (e.g., cancer cells), protection against autoimmune disorders and bacterial and viral infections, and neuro-muscular coordination. Low vitamin D levels may worsen certain disorders, including cancer, metabolic syndrome, obesity, T2D, infectious diseases, and autoimmune disorders. Whether increased incidences of these diseases are consequences of widespread vitamin D deficiency is not clear. However, many of the reported relationships between vitamin D deficiency and diseases are based on epidemiologic observations.

Measurement of serum 25(OH)D is the best way to evaluate vitamin D status. Serum 25(OH)D levels of less than 20 ng/mL are considered deficient, whereas optimum (physiological) blood levels are between 30 and 50 ng/mL. To achieve such levels, an additional 1,000 IU of vitamin D per day is sufficient for most lighter-skinned individuals, whereas elderly, obese, and dark-skinned individuals and other vulnerable groups of persons may need an additional 2,000 IU/day or more to maintain physiologic serum 25(OH) D levels.

Vitamin D inadequacy either precipitates or exacerbates several chronic diseases, including autoimmune disorders, insulin resistance, diabetes, and cardiovascular disease [33,100]. Other conditions also are linked to excess visceral fat [75]. Multiple mechanisms have been proposed for the observed relationship between obesity and vitamin D [102,103].

Altered vitamin D metabolism, abruption irregularities, and dilution of vitamin D within the excess fat mass of persons with obesity are some of the explanations provided for the low vitamin D status and need for larger doses of vitamin D supplements to increase serum vitamin D levels. Thus, vitamin D replacement therapy needs to be adjusted for body size to achieve the desired serum 25(OH)D concentrations [103]. Figure 2 illustrates correlations between vitamin D and obesity, T2D, metabolic syndrome, and osteoporosis.

Figure 2: The vitamin D triad: pathophysiological links between low vitamin D status and obesity, type 2 diabetes, metabolic syndrome, and osteoporosis.

Many studies have reported an inverse association between serum 25(OH)D levels and visceral adiposity [102,104,105] (Figure 1 & 2). The percentage of total body fat is also inversely correlated with the serum 25(OH)D levels [102,104,105]. Obese individuals have decreased bio-availability of vitamin D, thus necessitating higher doses of vitamin D [102]. Obese patients require two to four times greater vitamin D supplements to normalize their serum 25(OH)D levels than do non-obese patients. African-American patients with vitamin D deficiency have an additional inverse association with the amount of visceral fat and calcified atherosclerotic plaques [106,107].

Vitamin D deficiency, visceral fat and obesity

Vitamin D inadequacy is a risk factor for obesity (and vice versa) and related to associated disorders, including insulin resistance, hyperlipidemia, hypertension, diabetes, and sleep apnea, leading to increased incidence of CVD [38,75,108-117]. Those with the diagnosis of metabolic syndrome have significantly lower levels of serum 25(OH)D levels compared with those without the syndrome [100,115-117] (Figure 1). Excess visceral adiposity is positively correlated with insulin resistance, T2D, certain cancers, and premature deaths [118]. Evidence-based research on lifestyle interventions has demonstrated the effectiveness of such interventions in reducing insulin resistance [119], CVD, heart failure, stroke, cancer, diabetes, and all-cause mortality [120,121].

Although the mechanism for the association between obesity and vitamin D insufficiency is not well understood [4,97], researchers have suggested various mechanisms. Those who are obese are more likely to have vitamin D insufficiency [40,102], in part because of the combination of increased sequestration of vitamin D in excess visceral adipose tissue and dilutional [4,6] effects, but other mechanisms are also likely [102,103,116,117]. In addition, obese individuals need higher doses of vitamin D taken more frequently to attain and maintain their serum 25(OH)D levels than do individuals with normal BMI and normal waist circumference (WC) [2,33,35,36,38].

Association of serum 25(OH)D levels with visceral fat content

A number of studies have reported an inverse association of serum 25(OH)D levels and visceral body fat content: the higher the amount of visceral body fat, the lower the circulating 25(OH)D levels [122-124]. Moreover, ethnic minorities and persons with darker skin have a higher prevalence of vitamin D insufficiency than do their lighter-skinned counterparts [125] and are also known to have a high prevalence of abdominal obesity even with normal BMI. In addition to visceral fat, smoking, alcohol consumption, time spent outdoors, physical activity, occupation, menopausal status, intensity of skin color, cultural habits, exposure to solar ultraviolet B rays, and vitamin D supplement intake affect the serum 25(OH)D levels [4,97,126].

There is a high prevalence of vitamin D deficiency in those who are obese [2,46] and have metabolic syndrome [100]. Serum 25(OH)D levels not only provide surrogate information on visceral obesity [40] but also are a predictor of the levels of its active hormone, serum 1,25-dihydroxyvitamin D, in overweight and obese patients [33,34,36,127]. Vitamin D metabolism, storage, and biological action are all influenced by the visceral adiposity content. Higher visceral fat content is associated with a higher incidence of vitamin D deficiency. Figure 3 demonstrates the relationships of vitamin D deficiency with insulin resistance, metabolic syndrome T2D and obesity.

Figure 3: Inter-relationships between vitamin D deficiency with insulin resistance, metabolic syndrome T2D and obesity.

Association of vitamin D and insulin resistance

There is a strong association of vitamin D deficiency with insulin resistance, particularly in those with high visceral fat [38,44]. In addition, the amounts of visceral fat positively correlate with increase prevalence of impaired fasting glucose levels, abnormality of lipid metabolism, insulin resistance, hypertension, T2D, and a number of other metabolic risk factors [4,38,97,110-114,128,129].

High visceral fat content is positively correlated with vitamin D insufficiency and deficiency. Thus, the serum 25(OH)D levels can be used as a surrogate marker to quantitate functional visceral fat contents and together with the WC (or any of the quantitative methods for estimating visceral fat content) for estimating future risks of metabolic complications associated with obesity [55-57] (Figure 1 & 3).

Thus, the combination of the measurements of WC and serum 25(OH)D levels can be used to increase the sensitivity of detection and screening of people suspected of having excess visceral fat. Serum 25(OH)D and WC are easily measureable surrogate markers for identification of those with excess visceral adiposity and perhaps are a cost-effective aid in the identification of future metabolic risk associated with abdominal obesity and T2D.

Association of vitamin D deficiency and metabolic syndrome

Metabolic syndrome is a constellation of metabolic abnormalities, including abdominal obesity, insulin resistance, hypertension, prothrombotic profile, and chronic inflammation, that collectively increase the risks of T2D and associated complications, including CVD and premature death [130-132]. In most countries, the number of people with the aforementioned abnormalities has been increasing for the past three decades; such abnormalities are estimated to affect more than 40% of the US population.

Prolong vitamin D deficiency in the presence of excess visceral fat, increases calcium influx into adipocytes, further enhancing lipogenesis and secondarily, increase the production of parathyroid hormone [133-135]. The latter is a physiological attempt to correct vitamin D deficiency [2,127]. With reference to clinical studies that have used standard fixed doses of vitamin D supplementation in people with normal vitamin D levels without measuring their pre- and post-serum 25(OH)D levels, have not been able to demonstrate beneficial effects of vitamin D supplementation [1,136-138].


Compliance with instructions and medications is the key to successful weight loss; without compliance, the overall effectiveness of therapies for weight loss and improving metabolic syndrome is limited. Despite medical advances and the availability of new pharmaceutical agents, the prevention of obesity by lifestyle changes, healthy eating, and increased physical activity are the most cost-effective treatment and the fundamental basis for managing obesity. Positive lifestyle changes are essential for the longer-term success in weight maintenance of all persons who are obese, including those who embark on pharmacotherapy or bariatric surgery. Adherence to effective lifestyle changes with other medical means enables maintaining body weight at a lower physiological set point and minimizing the long-term complications of T2D and obesity.

Obese and overweight persons should be provided with advice and guidance on healthy lifestyle changes and the causes of weight gain in a given person, a weight-reducing diet plan to which the patient can adhere, a reasonable physical activity regimen, and monitoring of the patient’s progress. Since the diet provides little vitamin D, it is not that relevant to the vitamin D deficiency. However, the lifestyle is important, including outdoor leisure activities and sensible exposure to sunlight. Medications and bariatric surgery are effective but not the first set of options. Even when such treatments are offered, they must be complementary to lifestyle and behavioral changes [139].

In high-risk populations, timely and effective interventions would significantly reduce the human, social, and financial costs, as well as productivity lost from complications associated with metabolic syndrome and/or obesity. Testing for serum vitamin D levels should become a routine part of the managements and health maintenance of persons with metabolic syndrome, T2D, obesity, and osteoporosis.

Moreover, testing and treating for vitamin D deficiency would provide a real opportunity not only for cost-effective management of the deficiency in those who are at high risk but also for improving the health status of vulnerable populations and minimizing the need for universal supplementation. The use of serum 25(OH)D levels would increase the confidence of the diagnosis of visceral adiposity, allowing the taking of affirmative steps to rectify the problem. The combined use of abdominal circumference (WC) and serum 25(OH)D levels is more cost-effective in identifying or quantifying visceral adiposity and associated health risks than is relying on expensive lipid fraction studies and imaging methods.

Conflicts of Interest

The author has no conflicts of interest. There is no funding associated with this manuscript.


  1. Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, et al. (2011) Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 96(7): 1911-1930.
  2. Samuel L, Borrell LN (2013) The effect of body mass index on optimal vitamin D status in U.S. adults: the National Health and Nutrition Examination Survey 2001-2006. Ann Epidemiol 23(7): 409-414.
  3. Holick MF (2008) Deficiency of sunlight and vitamin D. BMJ 336(7657): 1318-1319.
  4. Wimalawansa SJ (2012) Vitamin D: Everything You Need to Know 2012. Karunaratne & Sons, Homagama, Sri Lanka.
  5. Zhen DLL, Guan C, Zhao N, Tang X (2015) High prevalence of vitamin D deficiency among middle-aged and elderly individuals in northwestern China: Its relationship to osteoporosis and lifestyle factors. Bone 71: 1-6.
  6. Wimalawansa SJ (2012) Vitamin D; What clinicians would like to know. Sri Lanka Journal of Diabetes, Endocrinology and Metabolism 1(2): 73-88.  
  7. Wimalawansa SJ (2014) Stigma of Obesity: A major barrier to overcome. Journal of Clinical & Translational Endocrinology 1: 73-76.
  8. Smith G, Wimalawansa SJ (2015) Reconciling the irreconcilable: micronutrients in clinical nutrition and public health. Vitamins & Minerals 4(1): 1-4.
  9. Quraishi SA, Bittner EA, Christopher KB, Camargo CA Jr (2013) Vitamin D status and community-acquired pneumonia: results from the third National Health and Nutrition Examination Survey. PLoS One 8(11): e81120.
  10. Caulfield LE, Stephanie A Richard, Juan A Rivera, Philip Musgrove, Robert E Black (2006) Stunting, Wasting, and Micronutrient Deficiency Disorders, in Disease Control Priorities in Developing Countries. In: DT Jamison, et al. (Eds.), Washington (DC).
  11. Sanchez-Castillo CP, Lara J, Romero-Keith J, Castorena G, Villa AR, et al. (2001) Nutrition and cataract in low-income Mexicans: experience in an Eye camp. Arch Latinoam Nutr 51(2): 113-121.
  12. Jahani R, Fielding KA, Chen J, Villa CR, Castelli LM, et al. (2014) Low vitamin D status throughout life results in an inflammatory prone status but does not alter bone mineral or strength in healthy 3-month-old CD-1 male mice. Mol Nutr Food Res 58(7): 1491-1501.
  13. Belenchia AM, Aneesh K Tosh, Laura S Hillman, Catherine A Peterson (2013) Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomized controlled trial. Am J Clin Nutr 97(4): 774-781.
  14. Awad AB, Alappat L, Valerio M (2012) Vitamin d and metabolic syndrome risk factors: evidence and mechanisms. Crit Rev Food Sci Nutr 52(2): 103-112.
  15. Roth CL, Elfers CT, Figlewicz DP, Melhorn SJ, Morton GJ, et al. (2012) Vitamin D deficiency in obese rats exacerbates nonalcoholic fatty liver disease and increases hepatic resistin and Toll-like receptor activation. Hepatology 55(4): 1103-1111.
  16. Ludvigsson J (2006) Why diabetes incidence increases--a unifying theory. Ann N Y Acad Sci 1079: 374-382.
  17. Kann L, Kinchen S, Shanklin SL, Flint KH, Harris WA, et al. (2014) Youth risk behavior surveillance--United States MMWR Surveill Summ 63 Suppl 4: 1-168.
  18. (2002) Centers for Disease C and Prevention, Prevalence of health-care providers asking older adults about their physical activity levels--United States, 1998. Morb Mortal Wkly Rep 51(19): 412-414.
  19. Ettner SL, Cadwell BL, Russell LB, Brown A, Safford M, et al. (2009) Investing time in health: do socioeconomically disadvantaged patients spend more or less extra time on diabetes self-care? Health Econ 18(6): 645-663.
  20. Bastida E, Pagan JA (2002) The impact of diabetes on adult employment and earnings of Mexican Americans: findings from a community based study. Health Econ 11(5): 403-413.
  21. Wimalawansa SJ (2014) Stigma of obesity: A major barrier to overcome. Journal of Clinical and Translational Endocrinology 1(3): 73-76.
  22. Hossain P, Kawar B, El Nahas M (2007) Obesity and diabetes in the developing world--a growing challenge. N Engl J Med 356(3): 213-215.
  23. Berrington de Gonzalez A, D Phil, Patricia Hartge, Sc D, James R, et al. (2010) Body-mass index and mortality among 1.46 million white adults. The New England Journal of Medicine 363(23): 2211-2219.
  24. Mousa A, Naderpoor N, Teede HJ, De Courten MP, Scragg R, et al. (2015) Vitamin D and cardiometabolic risk factors and diseases. Minerva Endocrinol 40(3): 213-230.
  25. Peterson CA, Tosh AK, Belenchia AM (2014) Vitamin D insufficiency and insulin resistance in obese adolescents. Ther Adv Endocrinol Metab 5(6): 166-189.
  26. Block G, Azar KM, Romanelli RJ, Block TJ, Hopkins D, et al. (2015) Diabetes Prevention and Weight Loss with a Fully Automated Behavioral Intervention by Email, Web, and Mobile Phone: A Randomized Controlled Trial Among Persons with Prediabetes. J Med Internet Res 17(10): e240.
  27. Baillot A, Audet M, Baillargeon JP, Dionne IJ, Valiquette L, et al. (2014) Impact of physical activity and fitness in class II and III obese individuals: a systematic review. Obes Rev 15(9): 721-739.
  28. Hammond RA, Levine R (2010) The economic impact of obesity in the United States. Diabetes Metab Syndr Obes 3: 285-295.
  29. de Ferranti SD, Gauvreau K, Ludwig DS, Neufeld EJ, Newburger JW, et al. (2004) Prevalence of the metabolic syndrome in American adolescents: findings from the Third National Health and Nutrition Examination Survey. Circulation 110(16): 2494-2497.
  30. Luger M, Kruschitz R, Marculescu R, Haslacher H, Hoppichler F, et al. (2015) The link between obesity and vitamin D in bariatric patients with omega-loop gastric bypass surgery - a vitamin D supplementation trial to compare the efficacy of postoperative cholecalciferol loading (LOAD): study protocol for a randomized controlled trial. Trials 16: 328.
  31. Wimalawansa SJ (2015) In the era of budgetary constraints, cost-Effective management of metabolic syndrome, type 2 diabetes, and obesity is essential. Cur Res Diabetes & Obesity J 1(1): 1-6.
  32. Delaet D, Schauer D (2011) Obesity in adults. BMJ Clin Evid.
  33. Reis AF, Hauache OM, Velho G (2005) Vitamin D endocrine system and the genetic susceptibility to diabetes, obesity and vascular disease. A review of evidence. Diabetes Metab 31(4 Pt 1): 318-325.
  34. Fox CS, Massaro JM, Hoffmann U, Pou KM, Maurovich-Horvat P, et al. (2007) Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study. Circulation 116(1): 39-48.
  35. Wimalawansa SJ (2014) Controlling obesity and its complications by elimination of causes and adopting healthy habits. Advances in Medical Sciences 3(1): 1-15.
  36. Lagunova Z, Porojnicu AC, Vieth R, Lindberg FA, Hexeberg S, et al. (2011) Serum 25-hydroxyvitamin D is a predictor of serum 1,25-dihydroxyvitamin D in overweight and obese patients. J Nutr 141(1): 112-117.
  37. WHO (2000) Obesity: preventing and managing the global epidemic. Report of a WHO consultation. World Health Organ Tech Rep Ser 1-253.
  38. Wimalawansa SJ (2015) Obesity and type 2 diabetes: preventing associated complications. Journal of Diabetes, Metabolic Disorders & Control 2(4): 1-4.
  39. Wimalawansa SJ (2013) Pathophysiology of obesity: Focused, cause-driven approach to control the epidemic. Global Advanced Research Journal of Pharmacy and Pharmacology 2(1): 1-13.
  40. Earthman CP, Beckman LM, Masodkar K, Sibley SD (2012) The link between obesity and low circulating 25-hydroxyvitamin D concentrations: considerations and implications. Int J Obes (Lond) 36(3): 387-396.
  41. Rodríguez-Rodríguez E, NLB, López-Sobaler AM, Ortega RM (2010) Associations between abdominal fat and body mass index on vitamin D status in a group of Spanish school children. Eur J Clin Nutr 64(5): 461-467.
  42. Xu L, Cheng X, Wang J, Cao Q, Sato T, et al. (2011) Comparisons of body-composition prediction accuracy: a study of 2 bioelectric impedance consumer devices in healthy Chinese persons using DXA and MRI as criteria methods. J Clin Densitom 14(4): 458-464.
  43. Gupta S, Kapoor S (2014) Body adiposity index: its relevance and validity in assessing body fatness of adults. ISRN Obes  243-294.
  44. Cornier MA, Després JP, Davis N, Grossniklaus DA, Klein S, et al. (2011) Assessing adiposity: a scientific statement from the American Heart Association. Circulation 124(18): 1996-2019.
  45. Wannamethee SG, Papacosta O, Whincup PH, Carson C, Thomas MC, et al. (2010) Assessing prediction of diabetes in older adults using different adiposity measures: a 7 year prospective study in 6,923 older men and women. Diabetologia 53(5): 890-898.
  46. Shoji K, Maeda K, Nakamura T, Funahashi T, Matsuzawa Y, et al. (2008) Measurement of visceral fat by abdominal bioelectrical impedance analysis is beneficial in medical checkup. Obes Res Clin Pract 2(4): p. I-II.
  47. Kuk JL, Lee S, Heymsfield SB, Ross R (2005) Waist circumference and abdominal adipose tissue distribution: influence of age and sex. Am J Clin Nutr 81(6): 1330-1334.
  48. Looker AC (2005) Body fat and vitamin D status in black versus white women. J Clin Endocrinol Metab 90(2): 635-640.
  49. Aronne LJ (2007) Therapeutic options for modifying cardiometabolic risk factors. Am J Med 120(3 Suppl 1): S26-S34.
  50. Neeland IJ, Ayers CR, Rohatgi AK, Turer AT, Berry JD, et al. (2013) Associations of visceral and abdominal subcutaneous adipose tissue with markers of cardiac and metabolic risk in obese adults. Obesity (Silver Spring) 21(9): E439-E447.
  51. Ross R, Despres JP (2009) Abdominal obesity, insulin resistance, and the metabolic syndrome: contribution of physical activity/exercise. Obesity (Silver Spring) 17 Suppl 3: S1-S2.
  52. Despres JP (1998) The insulin resistance-dyslipidemic syndrome of visceral obesity: effect on patients' risk. Obes Res 6(Suppl 1): 8S-17S.
  53. Engeli S, Negrel R, Sharma AM (2000) Physiology and pathophysiology of the adipose tissue renin-angiotensin system. Hypertension 35(6): 1270-1277.
  54. Yvan-Charvet L, Quignard-Boulange A (2011) Role of adipose tissue renin-angiotensin system in metabolic and inflammatory diseases associated with obesity. Kidney Int 79(2): 162-168.
  55. Wander PL, Boyko EJ, Leonetti DL, McNeely MJ, Kahn SE, et al. (2013) Change in visceral adiposity independently predicts a greater risk of developing type 2 diabetes over 10 years in Japanese Americans. Diabetes Care 36(2): 289-293.
  56. Bozorgmanesh M, Hadaegh F, Azizi F (2011) Predictive performance of the visceral adiposity index for a visceral adiposity-related risk: type 2 diabetes. Lipids Health Dis 10: 88.
  57. Du T, Sun X, Huo R, Yu X (2014) Visceral adiposity index, hypertriglyceridemic waist and risk of diabetes: the China Health and Nutrition Survey 2009. Int J Obes (Lond) 38(6): 840-847.
  58. Amato MC, Magistro A, Gambino G, Vesco R, Giordano C (2015) Visceral adiposity index and DHEAS are useful markers of diabetes risk in women with polycystic ovary syndrome. Eur J Endocrinol 172(1): 79-88.
  59. Russo GT, Labate AM, Giandalia A, Romeo EL, Villari P, et al. (2015) Twelve-month treatment with Liraglutide ameliorates Visceral Adiposity Index and common cardiovascular risk factors in type 2 diabetes outpatients. J Endocrinol Invest 38(1): 81-89.
  60. Ghanim H, Chaudhuri A, Dandona P (2010) Associations between dietary fiber and inflammation, hepatic function, and risk of type 2 diabetes in older men: potential mechanisms for the benefits of fiber on diabetes risk: response to wannamethee et Al. Diabetes Care 33(3): e43.
  61. Dandona P, Aljada A, Chaudhuri A, Mohanty P (2004) Endothelial dysfunction, inflammation and diabetes. Rev Endocr Metab Disord 5(3): 189-197.
  62. Dandona P, Aljada A, Chaudhuri A, Bandyopadhyay A (2003) The potential influence of inflammation and insulin resistance on the pathogenesis and treatment of atherosclerosis-related complications in type 2 diabetes. J Clin Endocrinol Metab 88(6): 2422-2429.
  63. Thethi TK, Bajwa MA, Ghanim H, Jo C, Weir M, et al. (2015) Effect of paricalcitol on endothelial function and inflammation in type 2 diabetes and chronic kidney disease. J Diabetes Complications 29(3): 433-437.
  64. Dandona P (2002) Endothelium, inflammation, and diabetes. Curr Diab Rep 2(4): 311-315.
  65. Dandona P, Aljada A, Bandyopadhyay A (2004) Inflammation: the link between insulin resistance, obesity and diabetes. Trends Immunol 25(1): 4-7.
  66. Krishnan AV, Feldman D (2011) Mechanisms of the anti-cancer and anti-inflammatory actions of vitamin d. Annu Rev Pharmacol Toxicol 51: 311-336.
  67. Zittermann A, Schleithoff SS, Koerfer R (2005) Putting cardiovascular disease and vitamin D insufficiency into perspective. Br J Nutr 94(4): 483-492.
  68. Adorini L, Amuchastegui S, Corsiero E, Laverny G, Le Meur T, et al. (2007) Vitamin D receptor agonists as anti-inflammatory agents. Expert Rev Clin Immunol 3(4): 477-489.
  69. Neyestani TR, Nikooyeh B, Alavi-Majd H, Shariatzadeh N, Kalayi A, et al. (2012) Improvement of Vitamin D Status via Daily Intake of Fortified Yogurt Drink Either with or without Extra Calcium Ameliorates Systemic Inflammatory Biomarkers, including Adipokines, in the Subjects with Type 2 Diabetes. J Clin Endocrinol Metab 97(6):2005.
  70. Chagas CE, Borges MC, Martini LA, Rogero MM (2012) Focus on vitamin D, inflammation and type 2 diabetes. Nutrients 4(1): 52-67.
  71. Ross R, Freeman J, Hudson R, Janssen I (2002) Abdominal obesity, muscle composition, and insulin resistance in premenopausal women. J Clin Endocrinol Metab 87(11): 5044-5051.
  72. Bacha F, Saad R, Gungor N, Janosky J, Arslanian SA (2003) Obesity, regional fat distribution, and syndrome X in obese black versus white adolescents: race differential in diabetogenic and atherogenic risk factors. J Clin Endocrinol Metab 88(6): 2534-2540.
  73. Boyko EJ, Leonetti DL, Bergstrom RW, Newell-Morris L, Fujimoto WY (1995) Visceral adiposity, fasting plasma insulin, and blood pressure in Japanese-Americans. Diabetes Care 18(2): 174-181.
  74. Boyko DJ, Fujimoto WY, Leonetti DL, Newell-Morris L (2000) Visceral adiposity and risk of type 2 diabetes - A prospective study among Japanese Americans. Diabetes Care 23(4): 465-471.
  75. Premanath M, Basavanagowdappa H, Mahesh M, Suresh M (2014) Correlation of abdominal adiposity with components of metabolic syndrome, anthropometric parameters and Insulin resistance, in obese and non obese, diabetics and non diabetics: A cross sectional observational study. (Mysore Visceral Adiposity in Diabetes Study). Indian J Endocrinol Metab 18(5): 676-682.
  76. Ducloux R, Nobécourt E, Chevallier JM, Ducloux H, Elian N, et al. (2011) Vitamin D deficiency before bariatric surgery: should supplement intake be routinely prescribed? Obes Surg 21(5): 556-560.
  77. Pittas AG, Lau J, Hu FB, Dawson-Hughes B (2007) The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis. J Clin Endocrinol Metab 92(6): 2017-2029.
  78. Lagunova Z, Porojnicu AC, Lindberg FA, Aksnes L, Moan J (2011) Vitamin D status in Norwegian children and adolescents with excess body weight. Pediatr Diabetes 12(2): 120-126.
  79. Zittermann A (2006) Vitamin D and disease prevention with special reference to cardiovascular disease. Prog Biophys Mol Biol 92(1): 39-48.
  80. Takiishi T, Gysemans C, Bouillon R, Mathieu C (2010) Vitamin D and diabetes. Endocrinol Metab Clin North Am 39(2): 419-446.
  81. Zeitz U, Karin Weber, Desi W, Soegiarto, Eckhard Wolf, et al. (2003) Impaired insulin secretory capacity in mice lacking a functional vitamin D receptor. FASEB J 17(3): 509-511.
  82. Jorde R, Sneve M, Emaus N, Figenschau Y, Grimnes G, et al. (2010) Cross-sectional and longitudinal relation between serum 25-hydroxyvitamin D and body mass index: the Tromso study. Eur J Nutr 49(7): 401-407.
  83. Elamin MB, Abu Elnour NO, Elamin KB, Fatourechi MM, Alkatib AA, et al. (2011) Vitamin D and cardiovascular outcomes: a systematic review and meta-analysis. J Clin Endocrinol Metab 96(7): 1931-1942.
  84. Palomer X, González-Clemente JM, Blanco-Vaca F, Mauricio D, et al. (2008) Role of vitamin D in the pathogenesis of type 2 diabetes mellitus. Diabetes Obes Metab 10(3): 185-197.
  85. Peechakara SV, Pittas AG (2008) Vitamin D as a potential modifier of diabetes risk. Nat Clin Pract Endocrinol Metab 4(4): 182-183.
  86. Di Cesar DJ, Ploutz-Snyder R, Weinstock RS, Moses AM (2006) Vitamin D deficiency is more common in type 2 than in type 1 diabetes. Diabetes Care 29(1): 174.
  87. Mathieu C, Badenhoop K (2005) Vitamin D and type 1 diabetes mellitus: state of the art. Trends Endocrinol Metab 16(6): 261-266.
  88. Mathieu C, Gysemans C, Giulietti A, Bouillon R (2005) Vitamin D and diabetes. Diabetologia 48(7): 1247-1257.
  89. Littorin B, Blom P, Schölin A, Arnqvist HJ, Blohmé G, et al. (2006) Lower levels of plasma 25-hydroxyvitamin D among young adults at diagnosis of autoimmune type 1 diabetes compared with control subjects: results from the nationwide Diabetes Incidence Study in Sweden (DISS). Diabetologia 49(12): 2847-2852.
  90. Choi HS, Kim KA, Lim CY, Rhee SY, Hwang YC, Kim KM, et al. (2011) Low serum vitamin D is associated with high risk of diabetes in Korean adults. J Nutr 141(8): 1524-1528.
  91. Gupta AK, Brashear MM, Johnson WD (2011) Prediabetes and prehypertension in healthy adults are associated with low vitamin D levels. Diabetes Care 34(3): 658-660.
  92. Hamed EA, Faddan NH, Elhafeez HA, Sayed D (2011) Parathormone - 25(OH)-vitamin D axis and bone status in children and adolescents with type 1 diabetes mellitus. Pediatr Diabetes 12(6): 536-546.
  93. Oh J, Weng S, Felton SK, Bhandare S, Riek A, et al. (2009) 1, 25(OH) 2 vitamin d inhibits foam cell formation and suppresses macrophage cholesterol uptake in patients with type 2 diabetes mellitus. Circulation 120(8): 687-698.
  94. Norman AW (2008) A vitamin D nutritional cornucopia: new insights concerning the serum 25-hydroxyvitamin D status of the US population. Am J Clin Nutr 88(6): 1455-1456.
  95. Holick MF (2006) High prevalence of vitamin D inadequacy and implications for health. Mayo Clin Proc 81(3): 353-373.
  96. Heaney RP (2005) The Vitamin D requirement in health and disease. J Steroid Biochem Mol Biol 97(1-2): 13-19.
  97. Wimalawansa SJ (2012) Vitamin D: An essential component for skeletal health. Annals of N Y Acad Sci 1240(1): 90-98.
  98. Hollis BW (2005) Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D. J Nutr 135(2): 317-322.
  99. Norman AW, Okamura WH, Bishop JE, Henry HL (2002) Update on biological actions of 1alpha, 25(OH)2-vitamin D3 (rapid effects) and 24R,25(OH)2-vitamin D3. Mol Cell Endocrinol 197(1-2): 1-13.
  100. Lu L, Yu Z, Pan A, Hu FB, Franco OH, et al. (2009) Plasma 25-hydroxyvitamin D concentration and metabolic syndrome among middle-aged and elderly Chinese individuals. Diabetes care 32(7): 1278-1283.
  101. Arunabh S, Pollack S, Yeh J, Aloia JF (2003) Body fat content and 25-hydroxyvitamin D levels in healthy women. J Clin Endocrinol Metab 88(1): 157-161.
  102. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF (2000) Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr 72(3): 690-693.
  103. Drincic AT, Armas LA, Van Diest EE, Heaney RP (2012) Volumetric Dilution, Rather Than Sequestration Best Explains the Low Vitamin D Status of Obesity. Obesity (Silver Spring) 20(7): 1444-1448.
  104. Caan B, Neuhouser M, Aragaki A, Lewis CB, Jackson R, et al. (2007) Calcium plus vitamin D supplementation and the risk of postmenopausal weight gain. Arch Intern Med 167(9): 893-902.
  105. Davidson MH, Hauptman J, DiGirolamo M, Foreyt JP, Halsted CH, et al. (1999) Weight control and risk factor reduction in obese subjects treated for 2 years with orlistat: a randomized controlled trial. JAMA 281(3): 235-242.
  106. Freedman BI, Wagenknecht LE, Hairston KG, Bowden DW, Carr JJ, et al. (2010) Vitamin d, adiposity, and calcified atherosclerotic plaque in african-americans. J Clin Endocrinol Metab 95(3): 1076-1083.
  107. Brenner DR, Arora P, Garcia-Bailo B, Wolever TM, Morrison H, et al. (2011) Plasma vitamin D levels and risk of metabolic syndrome in Canadians. Clin Invest Med 34(6): E377.
  108. Lee JH, O'Keefe JH, Bell D, Hensrud DD, Holick MF (2008) Vitamin D deficiency an important, common, and easily treatable cardiovascular risk factor? J Am Coll Cardiol 52(24): 1949-1956.
  109. Zittermann A, Frisch S, Berthold HK, Götting C, Kuhn J, et al. (2009) Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers. Am J Clin Nutr 89(5): 1321-1327.
  110. Yin X SQ, Zhang X, Lu Y, Sun C, Cui Y, et al. (2012) Serum 25(OH) D is inversely associated with metabolic syndrome risk profile among urban middle-aged Chinese population. Nutr J 11: 68
  111. Baker JF, Mehta NN, Baker DG, Toedter G, Shults J, et al. (2012) Vitamin D, metabolic dyslipidemia, and metabolic syndrome in rheumatoid arthritis. Am J Med 125(10): 1036e9-1036e15.
  112. Forouhi NG LJ, Cooper A, Boucher BJ, Wareham NJ (2008) Baseline serum 25-hydroxy vitamin D is predictive of future glycemic status and insulin resistance: the Medical Research Council Ely Prospective Study 1990-2000. Diabetes 57(10): 2619–2625.
  113. Hayashi T BE, Leonetti DL, McNeely MJ, Newell-Morris L, Kahn SE, et al. (2004) Visceral adiposity is an independent predictor of incident hypertension in Japanese Americans. Ann Intern Med 140(12): 992-1000.
  114. Goodpaster BH, KS, Resnick H, Kelley DE, Haggerty C, et al. (2003) Association between regional adipose tissue distribution and both type 2 diabetes and impaired glucose tolerance in elderly men and women. Diabetes Care 26(2): 372–379.
  115. Yoon H, KG, Kim SG, Moon AE (2015) The relationship between metabolic syndrome and increase of metabolic syndrome score and serum vitamin D levels in Korean adults. J Clin Biochem Nutr 57(1): 82-87.
  116. Wimalawansa SJ (2013) Thermogenesis based interventions for treatment for obesity and type 2 diabetes mellitus. Expert Reviews of Endocrinology & Metabolism 8(3): 275-288.
  117. Wimalawansa SJ (2013) Visceral adiposity and cardio-metabolic risks: Epidemic of Abdominal Obesity in North America. Research and Reports in Endocrine Disorders 3: 17-30.
  118. Renzaho AM, Halliday JA, Nowson C (2011) Vitamin D, obesity, and obesity-related chronic disease among ethnic minorities: A systematic review. Nutrition 27(9): 868-879.
  119. Jakicic JM, Jaramillo SA, Balasubramanyam A, Bancroft B, Curtis JM, et al. (2009) Effect of a lifestyle intervention on change in cardiorespiratory fitness in adults with type 2 diabetes: results from the Look AHEAD Study. Int J Obes (Lond) 33(3): 305-316.
  120. Kelly GS (2000) Insulin resistance: lifestyle and nutritional interventions. Altern Med Rev 5(2): 109-132.
  121. Cordain L, S Boyd Eaton, Anthony Sebastian, Neil Mann, Staffan Lindeberg, et al. (2005) Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr 81(2): 341-354.
  122. Eaton SB, Konner M (1985) Paleolithic nutrition. A consideration of its nature and current implications. N Engl J Med 312(5): 283-289.
  123. Zhang M, Li P, Zhu Y, Chang H, Wang X, et al. (2015) Higher visceral fat area increases the risk of vitamin D insufficiency and deficiency in Chinese adults. Nutr Metab (Lond) 12: 50.
  124. Sakamuri VP, Ananthathmakula P, Veettil GN, Ayyalasomayajula V, et al. (2011) Vitamin A decreases pre-receptor amplification of glucocorticoids in obesity: study on the effect of vitamin A on 11beta-hydroxysteroid dehydrogenase type 1 activity in liver and visceral fat of WNIN/Ob obese rats. Nutr J 10: 70.
  125. Fujimoto WY, Bergstrom RW, Boyko EJ, Chen K, Kahn SE, et al. (2000) Type 2 diabetes and the metabolic syndrome in Japanese Americans. Diabetes Res Clin Pract 50 Suppl 2: S73-S76.
  126. Grant WB, Wimalawansa SJ, Holick MF (2015) Vitamin D supplements and reasonable solar UVB should be recommended to prevent escalating incidence of chronic diseases. British Medical Journal 350: h321.
  127. Heaney RP (2011) Serum 25-hydroxyvitamin D is a reliable indicator of vitamin D status. Am J Clin Nutr 94(2): 619-620.
  128. Carr DB UK, Hull RL, Kodama K, Retzlaff BM, Brunzell J, et al. (2004) Intra-abdominal fat is a major determinant of the national cholesterol education program adult treatment panel III criteria for the metabolic syndrome. Diabetes 53(8): 2087-2094.
  129. Nagaretani HNT, Funahashi T, Kotani K, Miyanaga M, Tokunaga K, et al. (2001) Visceral fat is a major contributor for multiple risk factor clustering in Japanese men with impaired glucose tolerance. Diabetes Care 24(12): 2127-2133.
  130. Bagul PK, Middela H, Matapally S, Padiya R, Bastia T, et al. (2012) Attenuation of insulin resistance, metabolic syndrome and hepatic oxidative stress by resveratrol in fructose-fed rats. Pharmacol Res 66(3): 260-268.
  131. Du X, Greenfield H, Fraser DR, Ge K, Trube A, et al. (2001) Vitamin D deficiency and associated factors in adolescent girls in Beijing. Am J Clin Nutr 74(4): 494-500.
  132. Alemzadeh R, Kichler J (2012) Parathyroid hormone is associated with biomarkers of insulin resistance and inflammation, independent of vitamin D status, in obese adolescents. Metab Syndr Relat Disord 10(6): 422-429.
  133. McCarty MF, TC (2003) PTH excess may promote weight gain by impeding catecholamine-induced lipolysis-implications for the impact of calcium, vitamin D, and alcohol on body weight. Med Hypotheses 61(5-6): 535-542.
  134. Kim J (2015) Association between serum vitamin D, parathyroid hormone and metabolic syndrome in middle-aged and older Korean adults. Eur J Clin Nutr 69(4): 425-430.
  135. Ford ES, Zhao G, Li C, Pearson WS (2009) Serum concentrations of vitamin D and parathyroid hormone and prevalent metabolic syndrome among adults in the United States. J Diabetes 1(4): 296-303.
  136. Sneve M, Figenschau Y, Jorde R (2008) Supplementation with cholecalciferol does not result in weight reduction in overweight and obese subjects. Eur J Endocrinol 159(6): 675-684.
  137. Salehpour A, Shidfar F, Hosseinpanah F, Vafa M, Razaghi M, et al. (2012) Vitamin D3 and the risk of CVD in overweight and obese women: a randomised controlled trial. Br J Nutr 108(10): 1866-1873.
  138. Heaney R (2015) A statistical error in the estimation of the recommended dietary allowance for vitamin D. Nutrients 7(3): 1688-1690.
  139. Kramer H, Reboussin D, Bertoni AG, Marcovina S, Lipkin E, et al. (2009) Obesity and albuminuria among adults with type 2 diabetes: the Look AHEAD (Action for Health in Diabetes) Study. Diabetes Care 32(5): 851-853.
© 2014-2016 MedCrave Group, All rights reserved. No part of this content may be reproduced or transmitted in any form or by any means as per the standard guidelines of fair use.
Creative Commons License Open Access by MedCrave Group is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at
Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version | Opera |Privacy Policy