Diet and Inflammation - new insights into obesity and metabolic health
Published on 17 February 2011 in Food, health and wellbeing
Introduction
Until relatively recently, the predisposition of individuals to obesity was thought to be caused by a lack of will power in the face of a cheap and plentiful supply of highly palatable energy dense food. However, this type of diet, particularly one high in long chain saturated fat and sugary drinks, can also cause inflammation, which is now thought to play a role in the development of obesity.
Inflammation is most widely seen as the response to an infection or injury and clears up once the injury has healed or when the infection has passed. However, it appears that long chain saturated fatty acids can induce inflammation by stimulating the same receptors that respond to an infection, producing a low grade inflammation which persists.
It is thought that inflammation acting on the hypothalamic region of the brain may promote body weight gain and a decreased response to insulin, which are the first steps in developing type 2 diabetes.
Key Points
- Inflammation is central to obesity and many aspects of diet related ill health such as type 2 diabetes. Studies with mice have shown that blocking an inflammatory pathway can prevent the development of obesity and insulin insensitivity.
- Many researchers have focused on the role of long chain saturated fat itself in causing inflammation, but others think that these effects may be caused, at least in part, by microbial cell surface structures, especially lipopolysaccharide (LPS), also known as endotoxin, which is derived from Gram-negative bacteria mostly in the large intestine.
- High-fat diets promote passage of LPS into the bloodstream as they make the gut more permeable allowing LPS to enter the circulation. Sugary drinks are associated with increased levels of endotoxin in the circulation as they encourage bacterial overgrowth in the small intestine, an area where bacterial numbers are usually low. Also surprisingly certain highly processed foods have recently been shown to contain high levels of LPS which may impact on inflammation.
Research Undertaken
Diet induced obesity
Models of diet-induced obesity have been used to look at the effects of a high-fat diet and whether changes in the gut microbiota contribute to inflammation and insulin insensitivity. Mice on a high-fat diet very rapidly develop insulin insensitivity and we have shown that the initial response to this diet is an acute phase response which is equivalent to an infection. The appearance of immune cells – macrophages – in the fat of these animals is only seen after a prolonged period on the diet indicating that the source of the earlier inflammation is not the fat.
A high-fat diet changes the balance between different types of bacteria in the gut. These changes do not appear to favour increasing numbers of bacteria that cause inflammation but rather show a decrease in the number of bacteria that are important in maintaining gut integrity.
Possibilities for prebiotics
Work done in Belgium suggests that one of the mechanisms involved in maintaining gut integrity, is via the influence of short chain fatty acids (SCFAs) produced by microbial fermentation of fibres. Increasing dietary fibre will increase colonic SCFA concentrations, thus lowering the amount of LPS that passes into the bloodstream by reducing the permeability of the gut to large molecules like LPS. Recent work has demonstrated that this effect can be driven by increased SCFA production .Thus, by adding more non-digestible carbohydrates to the diet we can decrease the permeability of the gut and decrease inflammation (Research Brief: Probiotics and Prebiotics. Karen Scott)
Anti-inflammatory foods
The possibility that the incorporation into the diet of greater quantities of long chain n-3 polyunsaturated fatty acids (LC n-3 PUFA), fish oils, which have an anti inflammatory effect and may improve insulin sensitivity is also being tested. Metabolites of dietary LC n-3 PUFAs can ameliorate low-grade inflammation and improve insulin sensitivity. Recently a metabolite of EPA, termed resolvin has been demonstrated to effectively diminish inflammation in several animal models of disease. The potential role of this anti-inflammatory in obesity related inflammation has recently been investigated and indications are that it can reverse diet induced insulin resistance.
Policy Implications
This work adds further support to current advice to reduce dietary intake of saturated fats and sugary drinks, while increasing intake of oily fish and complex non-digestible carbohydrates. It also suggests possibilities for innovation in new product development.
Author
Lynda Williams l.williams@abdn.ac.uk
