Chronic antidiabetic and cardiovascular actions of leptin: role of CNS and increased adrenergic activity
Abstract
This study examined the importance of direct central nervous system (CNS) actions and increased adrenergic activity in mediating the chronic antidiabetic and cardiovascular actions of leptin. Insulin-deficient rats (streptozotocin, 50 mg/kg) were used to examine the effects of leptin on glucose homeostasis independent of changes in insulin. Male Sprague-Dawley rats were instrumented with arterial and venous catheters and intracerebroventricular cannula for 24-h/day blood pressure (BP) and heart rate (HR) monitoring and intravenous and intracerebroventricular infusions. Insulin-deficient diabetes was associated with marked hyperglycemia, hyperphagia, decreased BP, and pronounced fall in HR. Leptin treatment, intravenous or intracerebroventricular, completely restored to control values plasma glucose levels (384 ± 58 to 102 ± 28 and 307 ± 38 to 65 ± 7 mg/dl, respectively), food intake, BP, and HR (304 ± 8 to 364 ± 7 and 317 ± 13 to 423 ± 9 bpm, respectively). Combined blockade of α 1-, β 1-, and β 2-adrenergic receptors attenuated the rise in HR by 30 to 50% but had no effect on the antidiabetic and dietary actions of leptin. Blockade of β 3-adrenergic receptors did not attenuate the chronic cardiovascular or metabolic effects of leptin. These data demonstrate that leptin, via its direct actions in the CNS, has powerful antidiabetic actions in insulin-deficient rats independent of increased peripheral α 1, β 1, β 2, and β 3-adrenergic activity. Leptin also exerts important long-term cardiovascular actions that are partially mediated via α 1- and β 1/β 2-adrenergic activation. These findings provide new insights into novel pathways for long-term control of glucose homeostasis and cardiovascular regulation.
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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).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [43]
Activation of β3-adrenergic receptors is not required or sufficient to mediate the effects of leptin on blood glucose levels.
“nor was activation of the 3-adrenergic receptors required or sufficient to mediate the effects of leptin on blood glucose levels (7)”
From Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia (2011) · cites this paper as [7]
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Self-citation
- Authors
- da Silva, A. A., Tallam, L. S., Liu, J., & Hall, J. E.
- ORCID
- Hall, John E.
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2006-11
- Volume
- 291
- Issue
- 5
- Pages
- R1275-R1282
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- OpenAlex
- W2121512193
- Cited by
- 51
- References
- 36
- Citations by year
- 2026: 3 · 2024: 1 · 2022: 1 · 2021: 3 · 2020: 4 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 5 · 2014: 5 · 2013: 3 · 2012: 2
- FWCI
- 1.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01 HL-51972)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- leptin, insulin deficiency, streptozotocin-induced diabetes, glucose homeostasis, hyperglycemia, hyperphagia, blood pressure, heart rate, adrenergic receptors, alpha1-adrenoceptors, beta1-adrenergic receptor, beta2-adrenergic receptor, beta3-adrenergic receptor, central nervous system, intracerebroventricular infusion, cardiovascular regulation
- MeSH terms
- Animals, Blood Pressure, Cardiovascular Physiological Phenomena, Central Nervous System, Diabetes Mellitus, Experimental, Glucose, Heart Rate, Hemostasis, Insulin, Kidney, Male, Receptors, Adrenergic, Rats, Sprague-Dawley, Leptin, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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