Advances in ISSN: 2378-3168AOWMC

Obesity, Weight Management & Control
Volume 5 Issue 3 - 2016
Metabolic Disorders and Gut Microbiota
Tugba Cici*
Clinical Dietitian, Turkey
Received: November 14, 2016 | Published: November 25, 2016
*Corresponding author: Tugba Cici, Clinical Dietitian, Fulya Mah Hakki Yeten Caddesi, Vital Fulya Plaza No 23 Kat 334394 Fulya-Sisli, Istanbul, Turkey, Email:
Citation: Cici T (2016) Metabolic Disorders and Gut Microbiota. Adv Obes Weight Manag Control 5(3): 00133. DOI: 10.15406/aowmc.2016.05.00133


The burden of non-communicable diseases such as cardiovascular diseases, cancer, obesity and diabetes are leading causes of death and disability [1]. Recent studies in both rodents and humans indicate that the gut microbiota is also a contributor to metabolic disorders reviewed in [2]. Increased blood pressure, dyslipidemia (defined by increased triglycerides and reduced high-density lipoprotein cholesterol), elevated fasting blood sugar and central obesity are metabolic syndromes main features, as defined by the International Diabetes Federation (IDF) [3]. Recent evidences have proposed the potential role of gut microbiota as pathogenic factor affecting host metabolic balance and disorders [4].

Obesity is characterized by an excess of adipose tissue and occurs when an imbalance exists between energy intake and energy expenditure [5]. The onset of obesity is a complex process that involves genetic and environmental factors and is often associated with the development of several chronic complications, such as elevated fasting blood sugar (hyperglycemia), elevated triglyceride levels (hypertriglyceridemia), low levels of high density lipoprotein (dyslipidemia), and high blood pressure (hypertension) [6]. Individuals who meet at least three of these criteria are clinically diagnosed as having the metabolic syndrome [6], which increases the risk of developing metabolic disorders such as type 2 diabetes and cardiovascular diseases [7]. Most of the individuals with the metabolic syndrome have abnormal fat accumulation, which suggests that the excess of adipose tissue has a causative role in this syndrome [8].

Gut microbiota has recently been proposed as a crucial environmental factor driving metabolic disorders [9]. In fact, the gut microbiota is even seen as a separate endocrine organ, which is involved, through a molecular crosstalk with the host, in the maintenance of host energy homeostasis and in the stimulation of host immunity [10].

Shifts in gut microbial composition caused by external factors can result in a dramatic alteration of the symbiotic relationship between gut bacteria and the host, which promotes the development of metabolic disorders [11]. In particular, the gut microbiota is believed to contribute to metabolic disorders via stimulation of low-grade inflammation [12].

One of the hallmarks of obesity and obesity-related pathologies is the occurrence of chronic low-grade inflammation and low-grade inflammation causes various disorders [13]. Lipopolysaccharides (LPS), also called endotoxins, which are derived from the outer cell membrane of gram-negative bacteria, may trigger acute and chronic inflammation associated with the onset of obesity and insulin resistance [14].

The study of the metabolic, signalling, and immune interactions between gut microbes and the host, and how these interactions modulate host brain, muscle, liver and gut functions, has raised the concept of therapeutic microbial manipulation to combat or prevent metabolic disorders [15,16].

The use of probiotics and probiotics to improve the interactions between gut microbes and host metabolism in obesity and other metabolic disorders has been extensively investigated [17]. Probiotics are live microorganisms that, when used as food supplements, beneficially affect the host by improving the properties of the indigenous and changing the composition of the colonic microbiota [18].


  1. WHO (2005) Preventing Chronic Disease: a vital investment. WHO Global Report.
  2. Khan I, Harakeh SM, Kumosani T, Barbour E, Almasaudi SB, et al. (2016) Gut Microbiota: A Contributing Factor to Obesity. Front Cell Infect Microbiol 6: 95.
  3. The IDF consensus worldwide definition of the metabolic syndrome. International Diabetes Federation.
  4. Cani PD, Delzenne NM (2007) Gut microflora as a target for energy and metabolic homeostasis. Curr Opin Clin Nutr Metab Care 10(6): 729-734.
  5. World Health Organization (WHO) (2016) Obesity and overweight.
  6. Alberti KG, Zimmet P, Shaw J (2005) The metabolic syndrome-a new worldwide definition. Lancet 366(9491): 1059-1062.
  7. Iciar Martín-Timón, Cristina Sevillano-Collantes, Amparo Segura-Galindo, Francisco Javier del Cañizo-Gómez (2014) Type 2 diabetes and cardiovascular disease: Have all risk factors the same strength? World J Diabetes 5(4): 444-470.
  8. Despres JP, Lemieux I, Bergeron J, Pibarot P, Mathieu P, et al. (2008) Abdominal obesity and the metabolic syndrome: contribution to global cardio metabolic risk. Arterioscler Thromb Vasc Biol 28(6): 1039-1049.
  9. Claire L Boulangé, Ana Luisa Neves, Julien Chilloux, Jeremy K Nicholson, Marc-Emmanuel Dumas (2016) Impact of the gut microbiota on inflammation, obesity, and metabolic disease. Genome Medicine 8: 42.
  10. Clarke G, Stilling RM, Kennedy PJ, Stanton C, Cryan JF, et al. (2014) Mini review: Gut microbiota: the neglected endocrine organ. Mol Endocrinol 28(8): 1221-1238.
  11. Krajmalnik-Brown R, Ilhan ZE, Kang DW, DiBaise JK (2012) Effects of gut microbes on nutrient absorption and energy regulation. Nutr Clin Prac 27(2): 201-214
  12. Marchesi JR, Adams DH, Fava F, Hermes GD, Hirschfield GM, et al. (2016) The gut microbiota and host health: a new clinical frontier. Gut 65(2): 330-339.
  13. Gregor MF, Hotamisligil GS (2011) Inflammatory mechanisms in obesity. Annu Rev Immunol 29: 415-445.
  14. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, et al. (2007) Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 56(7): 1761-1772.
  15. Nicholson JK, Holmes E, Kinross J, Burcelin R, Gibson G, et al. (2012) Host-gut microbiota metabolic interactions. Science 336(6086): 1262-1267.
  16. Nicholson JK, Holmes E, Wilson ID (2005) Gut microorganisms, mammalian metabolism and personalized health care. Nat Rev Microbiol 3(5): 431-438.
  17. Kobyliak N, Conte C, Cammarota G, Haley AP, Styriak I, et al. (2016) Probiotics in prevention and treatment of obesity: a critical view. Nutr Metab (Lond) 13: 14.
  18. Hill C, Guarner F, Reid G, Gibson GR, Merenstein DJ, et al. (2014) Expert consensus document. The International Scientific Association for Probiotics and Probiotics consensus statement on the scope and appropriate use of the term probiotic. Nat Rev Gastroenterol Hepatol 11(8): 506-514.
© 2014-2018 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