Lep Ob Mice Research Articles

Leptin-deficient obese mice have altered intestinal metabolic enzyme activities

Introduction: Obesity is associated with multiple comorbidities, altered leptin metabolism, and increased intestinal absorption of nutrients. Leptin, the protein product of the mouse obese (ob) gene, inhibits carbohydrate absorption and improves the transport of oligopeptides across the intestinal epithelium via the PepT-1 transporter. Therefore, we hypothesized that leptin-deficient (Lepob) obese mice would have altered sucrase and brush border peptidase activities compared to lean controls. Methods: Sucrase and peptidase (aminopeptidase N (ApN), dipeptidyl peptidase IV (DPPIV)) activities were determined in jejunal and ileal segments from 16–18 week old male, lean control (C57BL/6J, n = 8) and leptin-deficient (Lepob, n = 8) obese mice. Data were analyzed using two-way ANOVA and Student-Newman-Keuls test for pair-wise multiple comparisons. Results: Lepob mice had significantly increased ileal (IL) sucrase activity and decreased jejunal (JE) ApN and DPPIV activity compared to lean controls. The activity for all three enzymes was greater in the jejunum than ileum for the lean control mice, whereas no difference was observed between the tissues for Lepob mice. Data (± SEM) are presented in the table below. Conclusions: These findings suggest 1) leptin deficient obese mice have greater absorption of carbohydrate in the ileum than lean controls and 2) diminished absorption for protein in the jejunum. Therefore, we conclude that the increased efficiency of carbohydrate absorption and not protein, may contribute to the obesity and diabetes evident in leptin-deficient obese mice. TABLE—ABSTRACT P58Strain/tissueSucrase (mcmol/cm/m in ×10−2)ApN (U/g)DPPIV (U/g)Lean/JE1.2 ± 0.1†17.3 ± 2.8†7.6 ± 0.5†Lean/IL0.5 ± 0.19.5 ± 2.83.9 ± 0.5Lepob/JE1.1 ± 0.19.6 ± 1.3∗4.0 ± 0.6∗Lepob/IL1.1 ± 0.1∗9.0 ± 0.72.5 ± 0.6∗P < 0.05 vs lean control.†P < 0.05 vs ileum same strain.

The forestomach of rats and mice, an effective device supporting digestive metabolism in muridae (review)

Summary The forestomach of rats and mice adapts the digestive regime of rats and mice from “food intake in bulks” to a “steady state digestion”. It stores well chewed and salivated food in amounts as needed for one to three hours or longer. The forestomach supplies its content for further digestion independently from its filling degree but in relation to the host's actual energy need during the light period or lipid metabolism during the dark period. Postprandial hyperglycemia and glycogen increase in the liver is lacking. Animals ingest most of their daily food during darkness. Meal frequency increases while the amount of food stored in the forestomach is hardly influenced. However, extremely high food demand or limitation of feeding time leads to increased filling per meal of the forestomach by four times and more, but in relation to “eating for calories”. The brain's appetite-regulating-network and signals which mechanically record the distension of the forestomach-stomach-cavity determine the ingested volume. In leptin-deficient Lep ob /Lep ob mice the filling volume of the forestomach per meal increases up to five times during the night and twice during the day. The frequency of meals declines. Emptying of the forestomach is controlled by a local feed back loop between duodenal reabsorption and the tension of the forestomach muscle fibres linked by humoral signals such as secretin and cholecystokinin. During storage in the forestomach food pap is subjected to digestion of starch, fat and chitin, but none of cellulose or protein can be observed. Microorganisms are without significance for the forestomach's function as shown in germ-free animals. Lactobacillae dominate in the variety of organisms lodged there. They are authochthonous and attached to the surface of the wall as dense carpets. Their lactic acid may have preservation effect on the food stored.