Department of Experimental Medical Science, Lund Univeristy
Abstract
Obesity is increasing throughout the world at an epidemic rate, partly due to increased consumption of diets rich in fat and/or sugar. Ghrelin and leptin are hormones, originating from the periphery, involved in the regulation of food intake and of maintaining energy homeostasis. Circulating ghrelin levels increase in times of energy deficiency, such as fasting, signalling hunger whereas circulating leptin levels increase during food intake, signaling termination of feeding. In rats offered a diet rich in sucrose, the pre- and postprandial difference in circulating leptin and ghrelin was abolished. This difference in leptin was also abolished in rats offered a high fat diet. Circulating concentrations of leptin was increased whereas ghrelin concentrations were decreased in the fasted state of rats offered a diet rich in both fat and sucrose. This suggests that the animals are trying to defend themselves against, or ameliorate the effects of, the energy-dense diets. This attempt to protect themselves is, however, not efficient enough to prevent the rats from overconsumption of the diets and gaining weight. Interestingly, fructose, a form of sugar very commonly used as a sweetener in soft drinks and other sweetened beverages, was found to increase fasting levels of ghrelin, thus promoting increased caloric consumption. The removal of the stomach (gastrectomy) in mice resulted in an 80% reduction in circulating ghrelin (hypoghrelinemia), in decreased amount of adipose tissue and decreased thermogenesis and ghrelin, when given daily over a period of eight weeks, normalised the amount of adipose tissue and thermogenesis in gastrectomised mice. A high fat diet was offered to rats in order to study the effect of such a diet on hippocampal neurogenesis. The high fat diet was found to impair neurogenesis in male rats, as indicated by a 40% reduction in newborn neurons. This effect was not observed in female rats. The high fat diet was also found to stimulate corticosterone in male rats (but not female rats), suggesting corticosterone to be responsible for the impairment in hippocampal neurogenesis
