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      Leptin and Hypertension in Obesity

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          Abstract

          Leptin, a peptide discovered more than 10 years ago, decreases food intake and increases sympathetic nerve activity to both thermogenic and nonthermogenic tissue. Leptin was initially believed to be an anti-obesity hormone, owing to its metabolic effects. However, obese individuals, for unknown reasons, become resistant to the satiety and weight-reducing effect of the hormone, but preserve leptin-mediated sympathetic activation to nonthermogenic tissue such as kidney, heart, and adrenal glands. Leptin has been shown to influence nitric oxide production and natriuresis, and along with chronic sympathetic activation, especially to the kidney, it may lead to sodium retention, systemic vasoconstriction, and blood pressure elevation. Consequently, leptin is currently considered to play an important role in the development of hypertension in obesity.

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          Leptin.

          R Ahima, J Flier (2000)
          The discovery of the adipose-derived hormone leptin has generated enormous interest in the interaction between peripheral signals and brain targets involved in the regulation of feeding and energy balance. Plasma leptin levels correlate with fat stores and respond to changes in energy balance. It was initially proposed that leptin serves a primary role as an anti-obesity hormone, but this role is commonly thwarted by leptin resistance. Leptin also serves as a mediator of the adaptation to fasting, and this role may be the primary function for which the molecule evolved. There is increasing evidence that leptin has systemic effects apart from those related to energy homeostasis, including regulation of neuroendocrine and immune function and a role in development.
          Article 0 comments Cited 272 times – based on 0 reviews     Review now
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            Region-specific leptin resistance within the hypothalamus of diet-induced obese mice.

            Heike Münzberg, Jeffrey Flier, Christian Bjørbaek (2004)
            Leptin resistance in diet-induced obese (DIO) mice is characterized by elevated serum leptin and a decreased response to exogenous leptin and is caused by unknown defects in the central nervous system. Leptin normally acts on several brain nuclei, but a detailed description of leptin resistance within individual brain regions has not been reported. We first mapped leptin-responsive cells in brains from DIO mice using phospho-signal transducer and activator of transcription (P-STAT3) immunohistochemistry. After 16 wk of high-fat-diet feeding, leptin-activated P-STAT3 staining within the arcuate nucleus (ARC) was dramatically decreased. In contrast, other hypothalamic and extrahypothalamic nuclei remained leptin sensitive. Reduced leptin-induced P-STAT3 in the ARC could also be detected after 4 wk and as early as 6 d of a high-fat diet. To examine potential mechanisms for leptin-resistant STAT3 activation in the ARC of DIO mice, we measured mRNA levels of candidate signaling molecules in the leptin receptor-STAT3 pathway. We found that the level of suppressor of cytokine signaling 3 (SOCS-3), an inhibitor of leptin signaling, is specifically increased in the ARC of DIO mice. The study suggests that the ARC is selectively leptin resistant in DIO mice and that this may be caused by elevated suppressor of cytokine signaling 3 in this hypothalamic nucleus. Defects in leptin action in the ARC may play a role in the pathogenesis of leptin-resistant obesity.
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              Receptor-mediated regional sympathetic nerve activation by leptin.

              Christine S. Walsh, D Morgan, William Sivitz … (1997)
              Leptin is a peptide hormone produced by adipose tissue which acts centrally to decrease appetite and increase energy expenditure. Although leptin increases norepinephrine turnover in thermogenic tissues, the effects of leptin on directly measured sympathetic nerve activity to thermogenic and other tissues are not known. We examined the effects of intravenous leptin and vehicle on sympathetic nerve activity to brown adipose tissue, kidney, hindlimb, and adrenal gland in anesthetized Sprague-Dawley rats. Intravenous infusion of mouse leptin over 3 h (total dose 10-1,000 microg/kg) increased plasma concentrations of immunoreactive murine leptin up to 50-fold. Leptin slowly increased sympathetic nerve activity to brown adipose tissue (+286+/-64% at 1,000 microg/kg; P = 0.002). Surprisingly, leptin infusion also produced gradual increases in renal sympathetic nerve activity (+228+/-63% at 1,000 microg/kg; P = 0.0008). The effect of leptin on sympathetic nerve activity was dose dependent, with a threshold dose of 100 microg/kg. Leptin also increased sympathetic nerve activity to the hindlimb (+287+/-60%) and adrenal gland (388+/-171%). Despite the increase in overall sympathetic nerve activity, leptin did not increase arterial pressure or heart rate. Leptin did not change plasma glucose and insulin concentrations. Infusion of vehicle did not alter sympathetic nerve activity. Obese Zucker rats, known to possess a mutation in the gene for the leptin receptor, were resistant to the sympathoexcitatory effects of leptin, despite higher achieved plasma leptin concentrations. These data demonstrate that leptin increases thermogenic sympathetic nerve activity and reveal an unexpected stimulatory effect of leptin on overall sympathetic nerve traffic.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Vasc Health Risk Manag
                Journal ID (publisher-id): Vascular Health and Risk Management
                Title: Vascular Health and Risk Management
                Publisher: Dove Medical Press
                ISSN (Print): 1176-6344
                ISSN (Electronic): 1178-2048
                Publication date (Print): June 2006
                Publication date (Electronic): June 2006
                Volume: 2
                Issue: 2
                Pages: 163-169
                Affiliations
                [1 ]Sections of Nephrology, Department of Internal Medicine, Louisiana State University Health Sciences Center New Orleans, LA, USA
                [2 ]Comprehensive Medicine, Department of Internal Medicine, Louisiana State University Health Sciences Center New Orleans, LA, USA
                Author notes
                Correspondence: Efrain Reisin, Chief of the Section of Nephrology, Department of Internal Medicine, Louisiana State University Health Sciences Center 1542 Tulane Avenue, New Orleans, LA 70112, USA Tel +1 504 568 8655 Fax +1 504 454 8218 Email ereisi@ 123456lsuhsc.edu .
                Article
                DOI: 10.2147/vhrm.2006.2.2.163
                PMC ID: 1993994
                PubMed ID: 17319461
                SO-VID: 7bdf2b54-e185-4a45-a1d3-3be8e9ef520a
                Copyright © © 2006 Dove Medical Press Limited. All rights reserved
                History
                Categories
                Subject: Review

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: nitric oxide,renal sympathetic nerve activity,obesity,blood pressure,leptin,selective leptin resistance,natriuresis
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: nitric oxide, renal sympathetic nerve activity, obesity, blood pressure, leptin, selective leptin resistance, natriuresis

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