Long-term effects of central leptin and resistin on body weight, insulin resistance, and β-cell function and mass by the modulation of hypothalamic leptin and insulin signaling.

Park, Sunmin; Hong, Sang Mee; Sung, So Ra; Jung, Hye Kyung

doi:10.1210/en.2007-0754

Cited by 73Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesPancreatic function and diabetes

Long-term effects of central leptin and resistin on body weight, insulin resistance, and β-cell function and mass by the modulation of hypothalamic leptin and insulin signaling.

Park, Sunmin, Hong, Sang Mee, Sung, So Ra, Jung, Hye Kyung·2008·Endocrinology

DOI 10.1210/en.2007-0754

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Abstract

To determine the long-term effect of central leptin and resistin on energy homeostasis, peripheral insulin resistance, and beta-cell function and mass, intracerebroventricular (ICV) infusion of leptin (3 ng/h), resistin (80 ng/h), leptin plus resistin, and cerebrospinal fluid (control) was conducted by means of an osmotic pump for 4 wk on normal rats and 90% pancreatectomized diabetic rats fed 40% fat-energy diets. Overall, the effects were greater in diabetic rats than normal rats. Leptin infusion, causing a significant reduction in food intake, decreased body weight and epididymal fat. However, resistin and leptin plus resistin reduced epididymal fat with decreased serum leptin levels in comparison with the control. Unlike serum leptin, only resistin infusion lowered serum resistin levels. Central leptin increased glucose infusion rates during euglycemic hyperinsulinemic clamp and suppressed hepatic glucose production in the hyperinsulinemic state in comparison with the control. However, central leptin did not affect glucose-stimulated insulin secretion and beta-cell mass. Central resistin infusion also increased peripheral insulin sensitivity, but not as much as leptin. Unlike leptin, resistin significantly increased first-phase insulin secretion during hyperglycemic clamp and beta-cell mass by augmenting beta-cell proliferation. These metabolic changes were associated with hypothalamic leptin and insulin signaling. ICV infusion of leptin potentiated signal transducer and activator of transcription 3 phosphorylation and attenuated AMP kinase in the hypothalamus, but resistin had less potent effects than leptin. Leptin enhanced insulin signaling by potentiating IRS2-->Akt pathways, whereas resistin activated Akt without augmenting insulin receptor substrate 2 phosphorylation. In conclusion, long-term ICV infusion of leptin and resistin independently improved energy and glucose homeostasis by modulating in different ways hypothalamic leptin and insulin signaling.

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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 [12]
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 [12]

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Authors: Park, S., Hong, S. M., Sung, S. R., & Jung, H. K.
Affiliations: Hoseo University (KR)
Corresponding author: Park, Sunmin
ORCID: Park, Sunmin
Jung, Hye Kyung
Venue: Endocrinology
Publisher: The Endocrine Society
Published: 2007-11-08
Volume: 149
Issue: 2
Pages: 445-454
ISSN: 0013-7227 (ISSN-L)
1945-7170
DOI: 10.1210/en.2007-0754
OpenAlex: W2024813257
Cited by: 73
References: 40
Citations by year: 2024: 3 · 2023: 2 · 2021: 3 · 2020: 2 · 2019: 4 · 2018: 2 · 2017: 4 · 2016: 4 · 2015: 5 · 2014: 5 · 2013: 4 · 2012: 7
FWCI: 2.72
Type: journal article
Language: en
Open access: closed
Locations: Endocrinology (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, resistin, insulin resistance, beta-cell function, beta-cell mass, energy homeostasis, glucose homeostasis, dietary intake, epididymal adipose tissue, hepatic glucose production, first-phase insulin secretion, beta-cell proliferation, AMP kinase, STAT3, intracerebroventricular infusion, diabetic rats, pancreatic resection
MeSH terms: Insulin Secretion, Animals, Blood Glucose, Body Weight, Cell Division, Eating, Glucose Tolerance Test, Hyperinsulinism, Hypothalamus, Injections, Intraventricular, Insulin, Insulin Resistance, Insulin-Like Growth Factor I, Male, Pancreatectomy, Glucose Clamp Technique, Signal Transduction, Rats, Sprague-Dawley, Apoptosis, Leptin, Insulin-Secreting Cells, Rats, Resistin

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Long-term effects of central leptin and resistin on body weight, insulin resistance, and β-cell function and mass by the modulation of hypothalamic leptin and insulin signaling.

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