Cheese-induced body weight gain is not accompanied by an increase of gastric cells producing leptin, ghrelin, gastrin, or pancreastatin in mice
The stomach is a source of several circulating peptides/hormones, such as gastrin, pancreastatin, leptin and ghrelin, which are thought to play important roles in the regulation of food intake and body growth. The present study was undertaken in mice in order to examine the effects of diet composition on the body weight gain and the gastric cells that produce these peptides/hormones.
Both young and adult female mice (BALB/cABBom strain) were given a standard pelleted dry diet, with or without cheese ad libitum, during a 7 week period. The diet supplement consisted either of carbohydrate- free white cheese containing 27% fat or sweet-tasting but sucrose-free Norwegian “brown cheese” containing 29% fat and 39% carbohydrate, mainly lactose. The total intake of the various types of food and the change in body weight were recorded. At the end of the observation period, blood samples were obtained for determination of gastric hormone levels by radioimmunoassay, and the stomachs were removed for examination of hormone producing cells by immunohistochemistry.
The young mice increased their body weight more than the adult mice. In the groups offered white cheese, both young and adult mice increased their body weight more than the animals kept on the standard diet alone. In contrast, the “brown cheese” supplement led to a relative overweight only in adult mice. Despite the changes in body weight gain, there were no differences with respect to the circulating levels of gastrin, leptin or ghrelin, and to the numbers of cells stained with antibodies to pancreastatin (including ECL cells and G cells), leptin (subpopulation of chief cells) and ghrelin (A-like cells) in all groups.
Body weight gain was increased in both young and adult mice by a white cheese diet supplement, whereas ‘brown cheese’ produced overweight only in adult mice. The increased body weight gain was not accompanied by an icrease of gastric cells producing leptin, ghrelin, gastrin, or pancreastatin.