According to the World Health Organization (WHO), we will have 700 million obese and 2.3 billion overweight people, worldwide, by the year 2015. Obesity stems from excessive intake of energy and/or storage of excess energy in adipose tissues. Numerous studies on obesity have focused on the role of the digestive, adipose and muscular systems. Emergent research shows how food can exert long-range effects on our brain, by at least four different mechanisms.

1. Regulation of appetite and fat metabolism by leptin and adiponectin (both are hormones involved in controlling appetite) is compromised in obese individuals. In individuals of normal body weight and metabolism, leptin is released by fat cells and sends signals of satiety to the brain. In obese individuals, one would postulate that a greater number of fat cells would ensure a greater amount of leptin released to facilitate ‘early’ satiety and reduced food intake. However, leptin does not work in this fashion in obese individuals and the answer to this conundrum is found in work conducted by researchers from University of Minnesota, Austin. Burguera and colleagues have shown that passage of leptin across the blood-brain barrier is impaired in obese rats. This work provides a clue as to why leptin resistance sets in, in obese individuals. This work also indicates why high levels of leptin are found in circulation in obese animals as well as people.

2. Saturated fats increase the levels of leptin in circulation. In mice, feeding on a diet rich in saturated fats for a week resulted in reduced expression of neuropeptide Y (NPY) gene in the hypothalamus region of the brain. Intake of a high-saturated fat diet for seven weeks resulted in elevated leptin levels in plasma with persistent changes in the expression patterns of NPY. Increased levels of Neuropeptide Y result in increased fat storage and energy intake. Ironically, although levels of expression of NPY were lowered in mice fed on saturated fats for a long time; these mice possessed increased fat mass and higher levels of leptin. The effect of a high-saturated-fat diet in these studies was specific to the kind of fats fed to the mice and not related to the amount of energy consumed. Polyunsaturated fats did not bring about similar metabolic changes in the brain as well as in circulating leptin levels. Experiments with animals fed a low-fat diet also showed similar results if the fats included in the diet were saturated fats. These results suggest that inclusion of saturated fats from sources like dairy, red meats and palm oil can affect the leptin signaling in the brain, leading to obesity. Palm oil is used in packaged foods and snacks.

3. Insulin is present and active in the cavities present in the brain (known as ventricles). Insulin plays a role in regulating appetite when it is acts on a region of the brain known as the hypothalamus. High intake of saturated fats like palmitic acid (present in palm oil) and stearic acid (present in red meat and cocoa butter) interferes with insulin signaling in the brain. These fatty acids also accumulate in the brain and create a physiological crisis situation known as inflammation. Together, these events disrupt regulation of food intake and promote obesity.

4. Consumption of a high-fat diet rich in saturated fats also has a detrimental effect in the generation of new brain cells. A region of the hippocampus, the dentate gyrus, is engaged in producing new brain cells. This regenerative activity is essential for long-term memory as well as cognitive functions. Recent research conducted at Pusan National University, Korea, shows that consumption of a diet rich in saturated fats hampers the production of new brain cells in the dentate gyrus. Cell division in this region of the brain is promoted by a growth factor known as Brain-Derived Neutrophic Factor (BDNF). A high-saturated fat diet results in reduced levels of BDNF and therefore slows down the process of cell division. Another harmful effect of this kind of diet is also the promotion of inflammation in the hippocampus. Excessive oxidation of fatty acids is seen in the hippocampus in animals exposed to this kind of diet.

A rationale for limiting consumption of dietary sources of saturated fats seems to be emerging from these studies.

References

Burguera B, Couce ME, Curran GL, Jensen MD, Lloyd RV, Cleary MP, & Poduslo JF (2000). Obesity is associated with a decreased leptin transport across the blood-brain barrier in rats. Diabetes, 49 (7), 1219-23 PMID: 10909981

Park HR, Park M, Choi J, Park KY, Chung HY, & Lee J (2010). A high-fat diet impairs neurogenesis: involvement of lipid peroxidation and brain-derived neurotrophic factor. Neuroscience letters, 482 (3), 235-9 PMID: 20670674

Posey KA, Clegg DJ, Printz RL, Byun J, Morton GJ, Vivekanandan-Giri A, Pennathur S, Baskin DG, Heinecke JW, Woods SC, Schwartz MW, & Niswender KD (2009). Hypothalamic proinflammatory lipid accumulation, inflammation, and insulin resistance in rats fed a high-fat diet. American journal of physiology. Endocrinology and metabolism, 296 (5) PMID: 19116375

Townsend KL, Lorenzi MM, & Widmaier EP (2008). High-fat diet-induced changes in body mass and hypothalamic gene expression in wild-type and leptin-deficient mice. Endocrine, 33 (2), 176-88 PMID: 18483882

Wang H, Storlien LH, & Huang XF (2002). Effects of dietary fat types on body fatness, leptin, and ARC leptin receptor, NPY, and AgRP mRNA expression. American journal of physiology. Endocrinology and metabolism, 282 (6) PMID: 12006366

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