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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 (Lep ob ) 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 (Lep ob , n = 8) obese mice. Data were analyzed using two-way ANOVA and Student-Newman-Keuls test for pair-wise multiple comparisons. Results: Lep ob 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 Lep ob 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 P58 . Strain/tissue Sucrase (mcmol/cm/m in ×10 −2 ) ApN (U/g) DPPIV (U/g) Lean/JE 1.2 ± 0.1 † 17.3 ± 2.8 † 7.6 ± 0.5 † Lean/IL 0.5 ± 0.1 9.5 ± 2.8 3.9 ± 0.5 Lep ob /JE 1.1 ± 0.1 9.6 ± 1.3 ∗ 4.0 ± 0.6 ∗ Lep ob /IL 1.1 ± 0.1 ∗ 9.0 ± 0.7 2.5 ± 0.6 ∗ P † P |
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