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Reduction of leptin levels by four cardiac hormones: Implications for hypertension in obesity

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      Abstract

      Circulating levels of leptin are increased in obesity and have been proposed to contribute to the development of hypertension in obese individuals. Four cardiac hormones, specifically, vessel dilator, long-acting natriuretic peptide (LANP), kaliuretic peptide and atrial natriuretic peptide (ANP), have blood pressure-lowering properties and correlate with the presence of hypertension in obesity. The objective of this study was to determine whether one or more of these cardiac hormones was able to decrease the levels of leptin in the hypothalamus, an area of the brain that has been demonstrated to synthesize more than 40% of leptin in the circulation. The effects of these four cardiac hormones on leptin were examined using dose-response curves in the rat hypothalamus, which synthesizes leptin. Vessel dilator, LANP, kaliuretic peptide and ANP maximally decreased the levels of leptin in hypothalamic cells by 79, 76, 80 and 62%, respectively (P<0.0001 for each). The cardiac hormones decreased leptin levels over a concentration range of 100 pM to 10 μM, with the most significant reductions in leptin levels occurring when the concentrations of the hormones were at micromolar levels. The results of the study suggest that the four cardiac hormones lead to significant reductions in hypothalamic leptin levels, which may be an important mechanism for alleviating leptin-induced hypertension in obesity.

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      Most cited references 42

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      Serum immunoreactive-leptin concentrations in normal-weight and obese humans.

      Leptin, the product of the ob gene, is a hormone secreted by adipocytes. Animals with mutations in the ob gene are obese and lose weight when given leptin, but little is known about the physiologic actions of leptin in humans. Using a newly developed radioimmunoassay, wer measured serum concentrations of leptin in 136 normal-weight subjects and 139 obese subjects (body-mass index, > or = 27.3 for men and > or = 27.8 for women; the body-mass index was defined as the weight in kilograms divided by the square of the height in meters). The measurements were repeated in seven obese subjects after weight loss and during maintenance of the lower weight. The ob messenger RNA (mRNA) content of adipocytes was determined in 27 normal-weight and 27 obese subjects. The mean (+/- SD) serum leptin concentrations were 31.3 +/- 24.1 ng per milliliter in the obese subjects and 7.5 +/- 9.3 ng per milliliter in the normal-weight subjects (P < 0.001). There was a strong positive correlation between serum leptin concentrations and the percentage of body fat (r = 0.85, P < 0.001). The ob mRNA content of adipocytes was about twice as high in the obese subjects as in the normal-weight subjects (P < 0.001) and was correlated with the percentage of body fat (r = 0.68, P < 0.001) in the 54 subjects in whom it was measured. In the seven obese subjects studied after weight loss, both serum leptin concentrations and ob mRNA content of adipocytes declined, but these measures increased again during the maintenance of the lower weight. Serum leptin concentrations are correlated with the percentage of body fat, suggesting that most obese persons are insensitive to endogenous leptin production.
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        Identification and expression cloning of a leptin receptor, OB-R.

        The ob gene product, leptin, is an important circulating signal for the regulation of body weight. To identify high affinity leptin-binding sites, we generated a series of leptin-alkaline phosphatase (AP) fusion proteins as well as [125I]leptin. After a binding survey of cell lines and tissues, we identified leptin-binding sites in the mouse choroid plexus. A cDNA expression library was prepared from mouse choroid plexus and screened with a leptin-AP fusion protein to identify a leptin receptor (OB-R). OB-R is a single membrane-spanning receptor most related to the gp130 signal-transducing component of the IL-6 receptor, the G-CSF receptor, and the LIF receptor. OB-R mRNA is expressed not only in choroid plexus, but also in several other tissues, including hypothalamus. Genetic mapping of the gene encoding OB-R shows that it is within the 5.1 cM interval of mouse chromosome 4 that contains the db locus.
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          Incidence and precursors of hypertension in young adults: the Framingham Offspring Study.

          The occurrence of hypertension and its precursors is examined in the Framingham Offspring Study of 2,027 men and 2,267 women ages 20-49 years followed for 8 years. The age-specific prevalence of hypertension was similar at both the first (1971-1975) and the second (1979-1983) examination for both men and women. Prevalence rates were higher among men than among women, and there was a higher rate of hypertension treatment at the second exam, particularly among women, 75% of whom reported being treated for hypertension. The incidence of hypertension in participants free from hypertension at the first examination increased threefold from the second to the fifth age decades in men and eight-fold in women. Under age 40, men were twice as likely as women to develop hypertension, but after age 40, 8-year incidence rates were similar in men (14.2%) and women (12.9%). Adiposity, relative weight, heart rate, alcohol intake, hematocrit, blood sugar, serum protein, triglyceride, and phosphorous were all related to hypertension occurrence in one or both sexes, controlling for age. In multivariate analysis, adiposity (P less than 0.01), heart rate (P less than 0.01), and triglyceride (P less than 0.05) were all significant independent predictors of hypertension in men. In women, adiposity (P less than 0.001), heart rate (P less than 0.01), hematocrit (P less than 0.05), and alcohol consumption (P less than 0.05) were independent contributors. When controlling for blood pressure measured at the first examination, the best single predictor of hypertension incidence, the multivariate assessment changed very little. Adiposity stands out as a major controllable contributor to hypertension. Changes in body fat over 8 years were related to changes in both systolic and diastolic blood pressure. Markedly obese women in their fourth decade were seven times more likely to develop hypertension than were lean women of the same age. Weight control deserves a high priority in efforts to prevent hypertension in the general population.
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            Author and article information

            Affiliations
            Departments of Medicine, Molecular Pharmacology and Physiology, and James A. Haley VA Medical Center, University of South Florida Morsani School of Medicine, Tampa, FL 33612, USA
            Author notes
            Correspondence to: Dr David L. Vesely, Departments of Internal Medicine, Molecular Pharmacology and Physiology, University of South Florida Morsani School of Medicine, 13000 Bruce B. Downs Boulevard, Tampa, FL 33612, USA, E-mail: david.vesely@ 123456va.gov
            Journal
            Exp Ther Med
            Exp Ther Med
            ETM
            Experimental and Therapeutic Medicine
            D.A. Spandidos
            1792-0981
            1792-1015
            August 2013
            21 June 2013
            21 June 2013
            : 6
            : 2
            : 611-615
            24137236 3786800 10.3892/etm.2013.1173 etm-06-02-0611
            Copyright © 2013, Spandidos Publications

            This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

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            Medicine

            leptin, cardiac hormones, hypertension in obesity, hypothalamus

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