Central Leptin Acutely Reverses Diet-Induced Hepatic Insulin Resistance
Open accessAbstract
Voluntary overfeeding rapidly induces resistance to the effects of systemic insulin and leptin on liver glucose metabolism. To examine whether central administration of recombinant leptin can restore leptin and insulin action on liver glucose fluxes, we infused leptin in the third cerebral ventricle of conscious overfed rats during pancreatic-insulin clamp studies. The effect of leptin on the phosphorylation of the signal transducer and activator of transcription-3 in the arcuate nuclei of the hypothalamus was similar in animals fed a regular diet or a high-fat diet for 3 days. The infusion of leptin in the third cerebral ventricle markedly inhibited glucose production in rats fed a high-fat diet mainly by decreasing glycogenolysis. The inhibition of glycogenolysis was sufficient to normalize glucose production and was accompanied by leptin-induced decreases in the hepatic expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. Thus central administration of leptin rescues the hepatic insulin resistance induced by short-term hyperphagia.
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This leptin action is distinct from its previously reported effect to increase insulin sensitivity in the liver and offers compelling evidence of a novel mechanism through which the brain normalizes diabetic hyperglycemia without the need for insulin.
“This leptin action is distinct from its previously reported effect to increase insulin sensitivity in the liver (66, 146), and offers compelling evidence of a novel mechanism through which the brain normalizes diabetic hyperglycemia without the need for insulin (67).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [146]
i.c.v. leptin infusion reverses insulin resistance induced by short-term high-fat diet by reducing both glycogenolysis and gluconeogenesis.
“i.c.v. leptin infusion reverses insulin resistance induced in rats by short-term exposure to a HF diet by reducing both glycogenolysis and gluconeogenesis (146)”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [146]
The antidiabetic effect of CNS leptin is distinct from leptin's previously reported effect to increase hepatic insulin sensitivity.
“This leptin action is distinct from its previously reported effect to increase insulin sensitivity in the liver and offers compelling evidence that the brain has the capacity to normalize diabetic hyperglycemia in the presence of sufficient amounts of central nervous system leptin.”
From Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia (2011) · cites this paper as [11]
Accumulating evidence suggests that leptin, insulin, and nutrient-related signals in the CNS improve hepatic insulin sensitivity.
“Although accumulating evidence suggests that leptin (10 -13), insulin (14,15), and nutrient-related signals (16 -18) in the CNS improve hepatic insulin sensitivity”
From Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia (2011) · cites this paper as [11]
Intracerebroventricular leptin can inhibit hepatic glucose production.
“and inhibit hepatic glucose production (Pocai et al., 2005; van den Hoek et al., 2008).”
From Leptin-Dependent Control of Glucose Balance and Locomotor Activity by POMC Neurons (2009) · cites this paper as Pocai et al., 2005
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References 43 · Cited by 153
- Authors
- Pocai, A., Morgan, K., Buettner, C., Gutierrez-Juarez, R., Obici, S., & Rossetti, L.
- Affiliations
- Albert Einstein College of Medicine (US)
- Departments of Medicine and Molecular Pharmacology, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-11-01
- Volume
- 54
- Issue
- 11
- Pages
- 3182-3189
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2140855423
- Cited by
- 153
- References
- 43
- Citations by year
- 2025: 1 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 3 · 2019: 6 · 2018: 6 · 2017: 10 · 2016: 6 · 2015: 10 · 2014: 7 · 2013: 9 · 2012: 16
- FWCI
- 3.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- Funders
- American Diabetes Association
- National Institutes of Health
- Albert Einstein College of Medicine, Yeshiva University
- National Institute on Aging (P01AG021654, AG 21654)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-48321, DK20541, DK-45024)
- 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, hepatic insulin resistance, diet-induced insulin resistance, high-fat diet, hyperphagia, glucose production, glycogenolysis, glucose-6-phosphatase, phosphoenolpyruvate carboxykinase, STAT3 phosphorylation, arcuate nucleus, hypothalamus, hepatic glucose metabolism
- MeSH terms
- Animals, Diet, Glucose, Hypothalamus, Insulin, Insulin Resistance, Liver, Male, Rats, Sprague-Dawley, Leptin, STAT3 Transcription Factor, Rats
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