A New Discovery in Obesity, Insulin Resistance, and Non-Alcoholic Fatty Liver Disease
If you find it almost impossible to lose weight or struggle with chronic obesity, your gut bacteria could be to blame. The inner ecology of your digestive system can directly influence serious health conditions like obesity and diabetes!
Recently, scientists have started to speculate that gut bacteria may play an essential role in the development of obesity, insulin resistance, and non-alcoholic fatty liver disease (NAFLD).1
You may not be familiar with NAFLD, but it is currently the most common liver disease worldwide, both in adults and in children, including 20% of the American population.2, 3
Gut bacteria may influence obesity and diabetes.
So far, instead of understanding what causes fatty liver, we only have a list of disorders that are associated with it. For example:
- Insulin resistance
- Obesity
- Hyperlipidemia, or high cholesterol
- Diabetes mellitus (type II)
- High blood pressure
Unhealthy Gut Bacteria Contribute to Weight Gain, Insulin Resistance, and NAFLD
As it turns out, gut bacteria can play a deciding role in whether or not an individual struggles with weight loss.
Studies have found that both obese mice and obese human beings are more likely to carry a specific type of bacteria.4, 5 On the other hand, mice and humans that are thin and slender have an entirely different microbial community populating the gut.6
As scientists looked deeper into the role that bacteria play in the development of obesity, they determined that changing the inner ecology of the gut with antibiotics, prebiotics, and probiotics can directly influence the development of obesity, diabetes, and NAFLD.7
Other studies have found that changing the gut bacteria in mice with insulin resistance creates NAFLD.8 Insulin resistance is often a precursor to type II diabetes.
more…
[+] Sources and References
1 E Vanni, et al. The gut-liver axis in nonalcoholic fatty liver disease: Another pathway to insulin resistance?. Hepatology. 2009; 49: 1790 – 1792. doi: 10.1002/hep.23036
2 M Lazo M, et al. Non-alcoholic fatty liver disease and mortality among US adults: prospective cohort study. BMJ. 2011; 343 (Nov 18): d6891. doi:10.1136/bmj.d6891
3 A Iacono, et al. Probiotics as an emerging therapeutic strategy to treat NAFLD: focus on molecular and biochemical mechanisms. The Journal of Nutritional Biochemistry. 2011 Aug; 22 (8): 699 – 711. doi:10.1016/j.jnutbio.2010.10.002
4 Backhed F, Ding H, Wang T, Hooper LV, Koh GY, Nagy A, et al. The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A 2004; 101: 15718–15723.
5 Ley RE, Backhed F, Turnbaugh P, Lozupone CA, Knight RD, Gordon JI. Obesity alters gut microbial ecology. Proc Natl Acad Sci U S A 2005; 102: 11070–11075.
6 Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesity-associated gut microbiome with increased capacity fro energy harvest. Nature 2006; 444: 1027–1031.
7 G Musso, et al. Gut microbiota as a regulator of energy homeostasis and ectopic fat deposition: mechanisms and implications for metabolic disorders. Lipidology. 2010 Feb; 21 (1): 76 – 83. doi: 10.1097/MOL.0b013e3283347ebb
8 ME Dumas, et al. Metabolic profiling reveals a contribution of gut microbiota to fatty liver phenotype in insulin-resistant mice. Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12511-6. Epub 2006 Aug 8. doi: 10.1073/pnas.0601056103
9 A. Abu-Shenab, et al. The role of the gut microbiota in nonalcoholic fatty liver disease. Nature Reviews Gastroenterology and Hepatology. 2010 Dec; 7, 691-701. doi:10.1038/nrgastro.2010.172
10 D Compare, et al. Gut–liver axis: The impact of gut microbiota on non alcoholic fatty liver disease. Nutrition, Metabolism and Cardiovascular Diseases. 2012 Jun; 22 (6): 471 – 476. doi: 10.1016/j.numecd.2012.02.007
11 DE Fouts, et al. Bacterial translocation and changes in the intestinal microbiome in mouse models of liver disease. J Hepatol. 2012 Jun;56(6):1283-92. Epub 2012 Feb 9.
12 E Albano, et al. Review article: role of oxidative stress in the progression of non-alcoholic steatosis. Alimentary Pharmacology & Therapeutics. 2005; 22: 71 – 73. doi: 10.1111/j.1365-2036.2005.02601.x
13 A Farhadi, et al. Susceptibility to gut leakiness: a possible mechanism for endotoxaemia in non-alcoholic steatohepatitis. Liver International, 2008; 28: 1026 – 1033. doi: 10.1111/j.1478-3231.2008.01723.x
14 L Miele, et al. Increased intestinal permeability and tight junction alterations in non-alcoholic fatty liver disease (NAFLD). Heptology. 2009. doi:10.1002/hep.22848.
15 AJ Wigg. The role of small intestinal bacterial overgrowth, intestinal permeability, endotoxemia, and tumour necrosis factor α in the pathogenesis of non-alcoholic steatohepatitis. Gut 2001; 48: 206–211.
16 Sajjad A, Mottershead M, Syn WK, Jones R, Smith S, Nwokolo CU. Ciprofloxacin suppresses bacterial overgrowth, increases fasting insulin but does not correct low acylated ghrelin concentration in non-alcoholic steatohepatitis. Aliment Pharmacol Ther 2005; 22: 291–299.
17 Sabaté JM, Jouët P, Harnois F, Mechler C, Msika S, Grossin M, et al. High prevalence of small intestinal bacterial overgrowth in patients with morbid obesity: a contributor to severe hepatic steatosis. Obes Surg 2008; 18: 371.
18 Y Sanz, et al. Probiotics as drugs against human gastrointestinal infections. Recent Pat Antiinfect Drug Discov. 2007 Jun;2(2):148-56.
19 L Abenavoli, et al. A pathogenetic link between non-alcoholic fatty liver disease and celiac disease. Endocrine. 2012. doi: 10.1007/s12020-012-9731-y
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