Altered intestinal motility in leptin-deficient obese mice1
| Autor: | Henry A. Pitt, James M. Kiely, Deborah A. Swartz-Basile, Shannon J. Graewin, Jae H. Noh |
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| Rok vydání: | 2005 |
| Předmět: |
medicine.medical_specialty
Gastrointestinal tract Liquid diet Leptin Deficiency Gastric emptying Stomach Leptin digestive oral and skin physiology Motility Biology Endocrinology medicine.anatomical_structure Internal medicine medicine Surgery hormones hormone substitutes and hormone antagonists Cholecystokinin |
| Zdroj: | Journal of Surgical Research. 124:98-103 |
| ISSN: | 0022-4804 |
| Popis: | Introduction Leptin is produced by adipocytes and causes satiety by regulating hypothalamic neurotransmission and energy expenditure. Leptin functions through the active long form of its receptor, which is expressed throughout the gastrointestinal tract, including the vagal neurons concerned with small intestinal motility. However, the role of leptin in small intestinal motility is poorly understood. Therefore, we hypothesized that leptin-deficient ( Lep ob ) obese mice would have altered small intestinal response to neurotransmitters and transit time. Materials and methods Responses of jejunal and ileal segments from lean control and leptin-deficient obese animals to acetylcholine (ACh) and cholecystokinin (CCK) were determined in an organ bath. In addition, gastric emptying was determined as the amount of gavaged liquid diet remaining in the stomach after 1 h, and intestinal transit time was determined by calculating the geometric center (GC) of passage of a fluorescent-labeled marker. Results Leptin deficiency resulted in increased jejunal responses to CCK ( P versus 91%, P versus 8.4, P versus 1.5, P Conclusions These studies indicate that leptin-deficient ( Lep ob ) obese mice have an increased jejunal response to CCK as well as an increased proximal intestinal transit, but an overall decrease in small intestinal transit. |
| Databáze: | OpenAIRE |
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