Cited by 124Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesPancreatic function and diabetes

Central leptin increases insulin sensitivity in streptozotocin-induced diabetic rats

Lin, Chia-Yu, Higginbotham, D. Allan, Judd, Robert L., White, B. Douglas·2002·American Journal of Physiology-Endocrinology and Metabolism

Abstract

This study examined the effect of intracerebroventricular leptin on insulin sensitivity in streptozotocin (STZ)-induced diabetic rats. Male Wistar rats were cannulated in the lateral ventricle and, after recovery, administered either intravenous STZ (50 mg/kg) to induce diabetes or citrate buffer. Chronic leptin (10 μg/10 μl icv) or vehicle injections were administered daily for 14 days beginning 2 days after establishment of hyperglycemia in the diabetic animals. At the end of the 2 wk of injections, insulin sensitivity was measured by the steady-state plasma glucose (SSPG) method. Blood glucose concentrations were dramatically reduced and normalized by the 4th day in diabetic animals receiving intracerebroventricular leptin treatment. Diabetic animals exhibited insulin resistance, whereas intracerebroventricular leptin significantly enhanced insulin sensitivity, as indicated by decreased SSPG. Circulating leptin levels were not increased in animals injected with intracerebroventricular leptin. Thus the increased peripheral insulin sensitivity appears to be due solely to the presence of leptin in the brain, not to leptin acting peripherally. These data imply that inadequate central leptin signaling may lead to insulin resistance.

Integrity signals

Registry

Crossref · 10.1152/ajpendo.00489.2001

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45 of 45 references verified0 citation errors · 0 not checkable

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  • Intracerebroventricular administration of leptin normalizes blood glucose levels in STZ-diabetic rats at doses that are ineffective when administered peripherally.

    “i.c.v. administration of leptin normalizes blood glucose levels in STZ-diabetic rats at doses that are ineffective when administered peripherally (43, 82, 104, 190).”

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Authors
Lin, C.-Y., Higginbotham, D. A., Judd, R. L., & White, B. D.
Affiliations
  • Department of Nutrition and Food Science, and
  • Auburn University (US)
Venue
American Journal of Physiology-Endocrinology and Metabolism
Published
2002-05-01
Volume
282
Issue
5
Pages
E1084-E1091
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
OpenAlex
W2122422623
Cited by
124
References
43
Citations by year
2025: 1 · 2024: 2 · 2023: 1 · 2022: 6 · 2021: 2 · 2020: 5 · 2019: 1 · 2018: 2 · 2017: 9 · 2016: 3 · 2015: 10 · 2014: 8 · 2013: 7 · 2012: 8
FWCI
2.11
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
leptin, insulin sensitivity, insulin resistance, streptozotocin-induced diabetes, blood glucose, hyperglycemia, type 2 diabetes
MeSH terms
Animals, Blood Glucose, Body Weight, Brain Chemistry, Diabetes Mellitus, Experimental, Eating, Fasting, Hyperglycemia, Injections, Intraventricular, Insulin, Insulin Resistance, Male, Signal Transduction, Rats, Wistar, Leptin, Rats

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