Acute stimulation of glucose metabolism in mice by leptin treatment
Abstract
Leptin is an adipocyte hormone that functions as an afferent signal in a negative feedback loop regulating body weight, and acts by interacting with a receptor in the hypothalamus and other tissues. Leptin treatment has potent effects on lipid metabolism, and leads to a large, specific reduction of adipose tissue mass after several days. Here we show that leptin also acts acutely to increase glucose metabolism, although studies of leptin's effect on glucose metabolism have typically been confounded by the weight-reducing actions of leptin treatment, which by itself could affect glucose homoeostasis. We have demonstrated acute in vivo effects of intravenous and intracerebroventricular administrations of leptin on glucose metabolism. A five-hour intravenous infusion of leptin into wild-type mice increased glucose turnover and glucose uptake, but decreased hepatic glycogen content. The plasma levels of insulin and glucose did not change. Similar effects were observed after both intravenous and intracerebroventricular infusion of leptin, suggesting that effects of leptin on glucose metabolism are mediated by the central nervous system (CNS). These data indicate that leptin induces a complex metabolic response with effects on glucose as well as lipid metabolism. This response is unique to leptin, which suggests that new efferent signals emanate from the CNS after leptin treatment.
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In wild-type mice, intravenous leptin increases glucose turnover and glucose uptake but decreases hepatic glycogen content.
“In wild-type mice, i.v. leptin increased glucose turnover and glucose uptake but decreased hepatic glycogen content (91).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [91]
The effect of leptin on glucose metabolism is similar whether leptin is administered intravenously or via intracerebroventricular infusion at much lower doses in both rats and mice.
“the effect is similar whether leptin is administered i.v. or via i.c.v. infusion (at much lower doses) in both rats (106) and mice (91).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [91]
At pharmacological doses, central administration of leptin in normal animals increases whole body glucose turnover and glucose uptake in skeletal muscle, heart, and brown adipose tissue, but not white adipose tissue, without changes in plasma insulin or glucose levels.
“at pharmacological doses, central administration of leptin in normal animals increases whole body glucose turnover and glucose uptake in peripheral tissues including skeletal muscle, heart and brown adipose tissue (BAT), but not white adipose tissue (WAT), without changes in plasma insulin or glucose levels (91).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [91]
Intracerebroventricular leptin can acutely stimulate glucose uptake in skeletal muscle.
“In addition, intracerebroventricular leptin can acutely stimulate glucose uptake in skeletal muscle (Cusin et al., 1998; Haque et al., 1999; Kamohara et al., 1997; Minokoshi et al., 1999)”
From Leptin-Dependent Control of Glucose Balance and Locomotor Activity by POMC Neurons (2009) · cites this paper as Kamohara et al., 1997
Central leptin administration can acutely increase muscle glucose uptake and decrease hepatic glucose production through altered autonomic output.
“Consistent with this, central leptin administration can acutely increase muscle glucose uptake (Kamohara et al., 1997) and decrease hepatic glucose production (van den Hoek et al., 2008) through altered autonomic output (Haque et al., 1999).”
From Leptin-Dependent Control of Glucose Balance and Locomotor Activity by POMC Neurons (2009) · cites this paper as Kamohara et al., 1997
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- Authors
- Kamohara, S., Burcelin, R., Halaas, J. L., Friedman, J. M., & Charron, M. J.
- Affiliations
- Rockefeller University (US)
- Albert Einstein College of Medicine (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Charron, Maureen J.
- Venue
- Nature
- Published
- 1997-09
- Volume
- 389
- Issue
- 6649
- Pages
- 374-377
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1580569338
- Cited by
- 708
- References
- 29
- Citations by year
- 2026: 1 · 2025: 11 · 2024: 10 · 2023: 7 · 2022: 10 · 2021: 13 · 2020: 16 · 2019: 11 · 2018: 17 · 2017: 27 · 2016: 20 · 2015: 30 · 2014: 25 · 2013: 28 · 2012: 25
- FWCI
- 13.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- 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 › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- leptin, glucose metabolism, glucose turnover, glucose uptake, liver glycogen, central nervous system, intracerebroventricular infusion, intravenous infusion, insulin, adipose tissue, lipid metabolism, glucose homeostasis, efferent signals
- MeSH terms
- Animals, Adipose Tissue, Brown, Central Nervous System, Denervation, Efferent Pathways, Glucose, Injections, Intravenous, Injections, Intraventricular, Insulin, Liver, Mice, Inbred C57BL, Proteins, Muscle, Skeletal, Leptin, Lipid Metabolism, Mice
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