Probiotics for Obesity and Metabolic Disorders

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Probiotics are well known for their use in gastrointestinal health, digestion, maturity of the innate immune system, reduction of systemic inflammation and the prevention of allergic conditions including asthma and atopy. Exciting new research is helping us understand how a broad spectrum probiotic may also play a role in the prevention and management of obesity and metabolic disorders.

Some of these fascinating findings include:

  • The probiotic colonies within the gut affect energy regulation.[1]
  • Probiotics and the short chain fatty acids (e.g. propionic acid) released by them may positively impact signals regulating appetite and metabolism.[2]
  • Obese individuals appear to have less bifidobacteria than their leaner counterparts.[3]
  • Probiotics improve hepatic fat metabolism via regulation of inflammation in the liver.[4,5]
  • A lactobacillus species was shown to lower abdominal obesity (both visceral and subcutaneous fat), increase adiponectin and alter other measures suggesting a beneficial influence on metabolic disorders.[6]
  • Probiotics reduce systemic inflammation and LPS known to be positively correlated with risk of insulin resistance.[4]
  • A bifidobacterium (B. lactis) species administered to diabetic mice resulted in improved fasting glycaemia, improved insulin secretion upon glucose challenge, showing improved glucose metabolism.
  • L. rhamnosus increased the synthesis of conjugated linoleic acid (CLA),[7] a fatty acid believed to influence adipokines and inflammatory mediators released from fat cells (adipocytes), reducing fat storage and associated inflammation.[8,9]

There are many factors that may contribute to obesity and metabolic syndrome. Firstly, the absence of energy homeostasis; when energy intake exceeds energy expenditure is a major cause. Secondly, numerous signals released from the gastrointestinal tract (e.g. CCK) and fat cells (adiponectin and leptin) interact to regulate hunger and metabolism. The liver plays a role in fat metabolism; and the absence of inflammation is important in the prevention of insulin resistance/type 2 diabetes, the regulation of appetite/metabolic signals and a range of factors associated with metabolic syndrome. Probiotics have demonstrated the ability to positively influence each and everyone of these aspects.[10,11One of the key mechanisms is via their anti-inflammatory mechanisms.

Inflammation causes weight gain and metabolic syndrome

Systemic inflammation may occur as a result of increased intestinal permeability (“leaky gut”). Increased intestinal permeability sees the increased passage of large proteins and pathogenic organisms into the body. Lipopolysaccharide (LPS) on these microorganisms initiate an immune-mediated inflammatory response, which may become widespread, or can also cause isolated inflammation in the liver. 

High levels of LPS and inflammation have been positively correlated with an increased risk of type 2 diabetes and metabolic syndrome. Elevated C-reactive protein (a marker of inflammation) has also shown the ability to interfere with the functioning of specific signals influencing appetite regulation and metabolism, and can compromise fat metabolism within the liver.[4]

Ultimately, chronic systemic inflammation will disrupt energy homeostasis and the metabolism of both sugars and fats within the body, the result is weight gain and metabolic disorders. 

Probiotics reduce inflammation and may prevent obesity and metabolic syndrome

Probiotics have the ability to reduce gastrointestinal permeability, and therefore controls the passage of pro-inflammatory LPS. They also express additional anti-inflammatory mechanisms via the release of anti-inflammatory cytokines.

As a result, the correction of dysbosis may improve the regulation of appetite and metabolism, maintaining healthy insulin sensitivity, improving liver function for fat metabolism and reducing the risk of additional co-morbidities of obesity and inflammation (i.e. metabolic syndrome).


  1. Cani PD, Delzenne NM. Interplay between obesity and associated metabolic disorders: new insights into the gut microbiota. Curr Opin Pharmacol. 2009 Dec;9(6):737-743. [Abstract]
  2. Al-Lahham SH, Roelofsen H, Priebe M, et al. Regulation of adipokine production in human adipose tissue by propionic acid. Eur J Clin Invest 2010;40(5):401-407. [Abstract]
  3. Santacruz A, Collado MC, Garcia-Valdes L, et al. Gut microbiota composition is associated with body weight, weight gain and biochemical parameters in pregnant women. Br J Nutr. 2010 Mar;1-10. [Abstract]
  4. Tsai F, Coyle WJ. The microbiome and obesity: is obesity linked to our gut flora? Curr Gastroenterol Rep. 2009;11(4):307-313. [Abstract]
  5. Gratz SW, Mykkanen H, El-Nezami HS. Probiotics and gut health: a special focus on liver diseases. World J Gastroentrol 2010;16(4):403-410. [Full text]
  6. Kadooka Y, Sato M, Imaizumi K, et al. Regulation of abdominal obesity by probiotics (Lactobacillus gasseri SBT2055) in adults with obese tendencies in randomized controlled trial. Eur J Clin Nutr 2010;64960:636-643. [Abstract]
  7. Lee HY, Park JH, Baek MW, et al. Human originated bacteria, Lactobacillus rhamnosus PL60, produce conjugated linoleic acid and show anti-obesity effects in diet-induced obese mice. Biochim Biophys Acta 2006;1761(7):736-744. [Abstract]
  8. Ocana A, Gomez-Asensio C, Arranz-Gutierrez E, et al. In vitro study of the effect of diesterified alkoxyglycerols with conjugated linoleic acid on adipocyte inflammatory mediators. Lipids Health Dis 2010;9:36. [Full text]
  9. Parra P, Palou A, Serra F. Moderate doses of conjugated linoleic acid reduce fat gain, maintain insulin sensitivity without impairing inflammatory adipose tissue status in mice fed high-fat diet. Nutr Metab (Lond) 2010;7:5. [Full text]
  10. Isolauri E, Kalliomaki M, Rautava S, et al. Obesity - extending the hygiene hypothesis. Nestle Nutr Workshop Ser Pediatr Program. 2009;64:75-85. [Abstract]
  11. Musso G, Gambino R, Cassader M. Gut microbiota as a regulator of energy homeostasis and ectopic fat deposition: mechanisms and implications for metabolic disorders. Curr Opin Lipidol. 2010;21(1):76-83. [Abstract]
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