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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0135v1 198/3/541    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wang, J. Articles by White, B. Search for Related Content PubMed PubMed Citation Articles by Wang, J. Articles by White, B.

J Wang, Nutrition and Food Science, Auburn University, Auburn, United States
C Wernette, Nutrition and Food Science, Auburn University, Auburn, United States
R Judd, Anatomy, Physiology and Pharmacology, Auburn University, Auburn, United States
K Huggins, Nutrition and Food Science, Auburn University, Auburn, United States
B White, Nutrition and Food Science, Auburn University, Auburn, United States

Correspondence: Barry White, Email: whitebd{at}auburn.edu

Abstract

Leptin, administered either into the ventricles of the brain or systemically, has been shown to normalize blood glucose concentrations in streptozotocin-induced diabetic rats. We hypothesized that an intact sympathetic nervous system is necessary for centrally administered leptin to normalize or attenuate high blood glucose concentrations in streptozotocin-induced diabetic rats. Young male Wistar rats (~ 50 g) were treated every other day with either subcutaneous guanethidine (100 mg/kg) or vehicle for 2 weeks. Rats were then implanted with an intracerebroventricular cannula directed to the lateral ventricle and made diabetic with an intravenous injection of streptozotocin (50 mg/kg). Half of the animals in each group were given daily injections of leptin (10 micrograms), while the remaining animals received vehicle injections. Blood glucose concentrations were measured daily and tissue norepinephrine content was determined by high performance liquid chromatography at the end of the study. Guanethidine pretreatment did not block the ability of centrally administered leptin to decrease blood glucose concentrations in diabetic rats. This suggests that the sympathetic nervous system does not mediate the leptin-induced attenuation of high blood glucose concentrations observed in diabetic rats.