Role of Leptin in the Regulation of Body Fluid Volume and Pressures

Guha, P. K.; Villarreal, Daniel; Reams, Garry P.; Freeman, Ronald H.

doi:10.1097/00045391-200305000-00008

Cited by 26 publications

(23 citation statements)

References 37 publications

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“…64,65 Leptin is likely to be involved in the pathogenesis of obesity hypertension, because it causes a significant increase in overall SNS activity, exerts a direct effect on the kidneys (resulting in increased sodium reabsorption) and regulates vasodilatation and vasoconstriction involving nitric oxidedependent and oxide-independent mechanisms. 62,66,67 In this study, plasma leptin significantly decreased after weight loss in patients with greater weight reduction and normalized BMI, which is consistent with previous observations. [68][69][70] Such a reduction in pL could have a role in the reducing BP values, which accompanied weight loss.…”

Section: Discussionsupporting

confidence: 92%

Effect of body weight loss and normalization on blood pressure in overweight non-obese patients with stage 1 hypertension

et al. 2010

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We evaluated the effects of body weight (BW) loss on blood pressure (BP) in overweight non-obese patients with stage 1 hypertension. We enrolled 376 overweight (body mass index (BMI) X25 and o30 kg m À2 ) stage 1 hypertensive patients in this prospective 12-month trial. Each patient received tailored, low caloric dietary advice. After 6 months, patients with a BW reduction o5% were excluded. Body weight, BMI, BP, fasting plasma glucose (FPG), fasting plasma insulin (FPI), leptin (pL), renin and aldosterone levels were evaluated at baseline and after 6 and 12 months. In 222 patients who completed the study, a mean weight reduction of 8.1 kg reduced systolic blood pressure (SBP) by 4.2 mm Hg and diastolic blood pressure (DBP) by 3.3 mm Hg (Po0.05), which was accompanied by a significant decrease in FPI, pL and aldosterone levels (Po0.05). Larger SBP/DBP reductions were observed in 106 patients with normalized BMI (À5/À4.5 mm Hg, Po0.01) compared with the 116 patients who did not become normalized (À3.3/À1.6 mm Hg). The former also presented with greater decreases in FPG, FPI, pL, renin and aldosterone levels. Of the 106 patients who had normalized BMI, 52 also had normalized BP. Clinical and metabolic characteristics of these patients were similar to those of the 56 patients who did not have normalized BP. In overweight, mild hypertensive patients, weight loss was effective in reducing BP and in reversing some endocrinologic alterations associated with being overweight. Half of the patients who had normalized BMI also had normalized BP, which could indicate that these patients essentially did not have a form of hypertension but that these effects were instead secondary to being overweight. Keywords: blood pressure; overweight; weight-loss INTRODUCTION Excessive body weight (BW), in particular abdominal obesity, increases the risk for cardiovascular disease, stroke, type 2 diabetes, hypertension, lipoprotein disorders, osteoarthritis, certain types of cancers and total mortality. 1-5 An escalating epidemic of overweight (body mass index (BMI) X25 and o30 kg m À2 ) and obesity (BMI 430 kg m À2 ), is affecting both industrialized and many developing countries in the world, and constitutes a major public health problem. 4,6,7 In particular, in the United States, the prevalence of obesity was estimated at 32% of the population. Being overweight was even more prevalent, representing 42% of men and 28% of women, of whom 34 and 39%, respectively, had high blood pressure (BP). 8,9 The coexistence of hypertension and excessive BW greatly enhances cardiovascular risk. 2,10 Recent recommendations suggest the use of stratification tables to calculate the percentage of increased cardiovascular risk in patients with hypertension and excess BW or obesity. 11 The mechanisms underlying hypertension in subjects with excessive BW

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Section: Discussionsupporting

confidence: 92%

Effect of body weight loss and normalization on blood pressure in overweight non-obese patients with stage 1 hypertension

et al. 2010

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“…Leptin, the ob gene product, is a 16-kDa, primarily white adipose tissue-derived circulating hormone (Bates and Myers, 2003;Guha et al, 2003;Pico et al, 2003) that acts as a lipostatic negative feedback signal to regulate energy balance. With increasing fat stores, circulating leptin levels increase to curb appetite and facilitate energy utilization (Bates and Myers, 2003).…”

Section: Discussionmentioning

confidence: 99%

Opioid-Dependent Anticipatory Negative Contrast and Binge-Like Eating in Rats with Limited Access to Highly Preferred Food

Cottone

Sabino

Steardo

et al. 2007

Neuropsychopharmacol

131

149

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Binge eating and an increased role for palatability in determining food intake are abnormal adaptations in feeding behavior linked to eating disorders and body weight dysregulation. The present study tested the hypothesis that rats with limited access to highly preferred food would develop analogous opioid-dependent learned adaptations in feeding behavior, with associated changes in metabolism and anxiety-like behavior. For this purpose, adolescent female Wistar rats were daily food deprived (2 h) and then offered 10-min access to a feeder containing chow followed sequentially by 10-min access to a different feeder containing either chow (chow/chow; n ¼ 7) or a highly preferred, but macronutrient-comparable, sucrose-rich diet (chow/preferred; n ¼ 8). Chow/preferred-fed rats developed binge-like hyperphagia of preferred diet from the second feeder and anticipatory chow hypophagia from the first feeder with a time course suggesting associative learning. The feeding adaptations were dissociable in onset, across individuals, and in their dose-response to the opioid-receptor antagonist nalmefene, suggesting that they represent distinct palatability-motivated processes. Chow/preferred-fed rats showed increased anxiety-like behavior in relation to their propensity to binge as well as increased feed efficiency, body weight, and visceral adiposity. Chow/preferred-fed rats also had increased circulating leptin levels and decreased growth hormone and 'active' ghrelin levels. Thus, the short-term control of food intake in rats with restricted access to highly preferred foods comes to rely more on hedonic, rather than nutritional, properties of food, through associative learning mechanisms. Such rats show changes in ingestive, metabolic, endocrine, and anxiety-related measures, which resemble features of binge eating disorders or obesity.

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“…8,30,31 Accordingly, leptin has been considered a systemic sympathetic-mediated pressor lever resembling the clinical model of obesity-related hypertension. 8 On the other way around, it is yet unresolved whether the increased hemodynamic load, per se, promotes hyperleptinemia 32,33 or whether a functional intermediate link, eg, subclinical inflammation 5,6 and/or endothelial dysfunction, [12][13][14]34 could separately or in combination contribute to the association proposed by the present study.…”

Section: Discussionmentioning

confidence: 99%

Free Leptin Is Associated With Masked Hypertension in Nonobese Subjects

et al. 2009

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Abstract-The aim of the study was to investigate whether diverse clinical blood pressure phenotypes are associated with free leptin surrogates, as reflected by plasma leptin, human soluble leptin receptor, and their ratio (ie, free leptin index) in nonobese normoglycemic subjects. Three separate clinic blood pressure measurements and ambulatory blood pressure monitoring were implemented to divide 494 subjects (aged 44Ϯ5 years; 272 men; body mass index: Ͻ30 kg/m 2 ) into hypertensives (nϭ166), white-coat hypertensives (nϭ82), masked hypertensives (nϭ66), and normotensives (nϭ180). Participants underwent echocardiography, while, from fasting venous blood samples, metabolic profile, plasma leptin, and its receptor levels were assessed. Hypertensives and masked hypertensives demonstrated higher levels of log (10)(leptin) and log (10)(free leptin index), as well as lower levels of log (10)(human soluble leptin receptor) with respect to normotensives. White-coat hypertensives had similar free leptin surrogates compared with normotensives. Younger age, 24-hour systolic and diastolic blood pressures, 24-hour heart rate, and left ventricle mass index were common correlates of free leptin surrogates. After adjustment for confounders, masked hypertensive and hypertensive with respect to normotensive phenotype were associated with log (10)(leptin) with odds ratios (95% CIs) of 1.31 (1.12 to 3.80) and 1.26 (1.09 to 2.24), respectively, log (10)(human soluble leptin receptor) with 0.65 (0.53 to 0.78) and 0.69 (0.57 to 0.84), respectively, and log (10)(free leptin index) with 2.46 (1.32 to 7.23) and 1.84 (1.26 to 3.73), respectively (PϽ0.05 for all of the cases). Free leptin surrogates are associated with masked hypertension in nonobese normoglycemic subjects. Free leptin is almost equally increased in masked and sustained hypertension, suggesting a similar leptin-related vascular impairment. ncreased leptin levels have been independently associated with cardiovascular diseases 1 and risk factors such as obesity, insulin resistance, type 2 diabetes mellitus, 2 as well as with blood pressure (BP) levels even below the clinically defined hypertensive cutoff value. 3,4 Leptin may be implicated on the perpetuation of systemic inflammation given its modulator effect on C-reactive protein 5 and its structural and functional resemblance to proinflammatory cytokines like interleukin 6. 6 Because between hypertension and systemic inflammation there is an established reciprocal pathophysiological link, 7 hyperleptinemia might be implicated on the adverse hemodynamic regulation beyond the centrally obesity-mediated mechanisms of leptin resistance. 8 Although in vivo studies supported the notion that chronic hemodynamic actions of leptin are likely attributable to widespread sympathoactivation of metabolically active tissues and not to the vasculature to increase vasomotor tone, 9 in vitro evidence suggested that leptin at concentrations higher than the physiologically relevant level may exert adverse effects on the vasculature by periphe...

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Role of Leptin in the Regulation of Body Fluid Volume and Pressures

Cited by 26 publications

References 37 publications

Effect of body weight loss and normalization on blood pressure in overweight non-obese patients with stage 1 hypertension

Effect of body weight loss and normalization on blood pressure in overweight non-obese patients with stage 1 hypertension

Opioid-Dependent Anticipatory Negative Contrast and Binge-Like Eating in Rats with Limited Access to Highly Preferred Food

Free Leptin Is Associated With Masked Hypertension in Nonobese Subjects

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