Obesity hypertension: the emerging role of leptin in renal and cardiovascular dyshomeostasis

Kshatriya, Shilpa; Reams, Garry P.; Spear, Robert M.; Freeman, Ronald H.; Dietz, John R.; Villarreal, Daniel

doi:10.1097/mnh.0b013e328332fb49

Cited by 22 publications

(17 citation statements)

References 79 publications

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“…Recent evidence, however, suggests that leptin's actions are not necessarily impaired across all of its domains. In particular, stimulatory effects of leptin on blood pressure are observed in obesity (4,5). Higher levels of leptin in obese individuals have been associated with increased blood pressure and increased cardiovascular disease risk (6).…”

Section: Discussionmentioning

confidence: 99%

“…There is evidence to suggest, however, that not all of leptin's actions are altered in obesity. The stimulatory effect of leptin on the sympathetic nervous system and subsequently increased blood pressure (3), for example, appears intact (4,5), which may explain the association between higher leptin levels and increased risk of hypertension in obese adults (4,6). Thus, hyperleptinemia in obese individuals could have important consequences for cardiovascular health independently of body weight.…”

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confidence: 99%

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No Association Between Leptin Levels and Sleep Duration or Quality in Obese Adults

Knutson

Galli

Zhao

et al. 2011

Obesity

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Previous research in lean subjects has found lower leptin levels associated with shorter sleep duration. Since leptin levels are higher and some of the actions of leptin are impaired in obese individuals, one cannot assume that sleep will be similarly associated with leptin in obese individuals. The aim of this paper was to examine the cross-sectional association between habitual sleep duration and quality and plasma leptin levels in a sample of 80 obese men and premenopausal women aged 18–50 years. Leptin levels (ng/ml) were assayed on a fasting blood sample taken in the morning. We calculated a relative leptin level by dividing leptin by body fat percentage. Sleep duration and sleep efficiency were measured by 2 weeks of wrist actigraphy and respiratory disturbance index (RDI), a measure of sleep disordered breathing, was assessed by a portable screening device on a single night. Mean leptin levels and body fat percentage were higher in women than men (P < 0.001), however, mean RDI was higher in men (P = 0.01). There were no significant associations between relative leptin level and any of the sleep measures, including sleep duration, sleep efficiency, and sleep disordered breathing. There was also no difference between men and women in the association between sleep and leptin. In conclusion, contrary to what has been reported in other studies, measures of sleep duration and quality were not associated with leptin levels in our sample of obese adults.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

No Association Between Leptin Levels and Sleep Duration or Quality in Obese Adults

Knutson

Galli

Zhao

et al. 2011

Obesity

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“…Taken together, activation of the sympathetic nervous system is an important factor in the onset and development of obesity-related renal injury, 7,20,22,23 and hence WL Renal function during weight loss K Masuo et al programs should be initiated and convey some degree of renal protection in the overweight/obese patient. Glomerular hyperfiltration, 41 hyperleptinemia, 43,44 insulin resistance 30 and stimulation of the RAS, 21,45 accompanying heightened sympathetic nervous activity, may contribute to renal injury in obesity. It has been documented that the RAS is linked to obesity and its activity is reduced in association with WL.…”

Section: Discussionmentioning

confidence: 99%

Effects of weight loss on renal function in overweight Japanese men

et al. 2011

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Obesity is known as an independent risk factor for renal injury. Sympathetic nerve activation may have an important role of the pathogenesis of obesity, and hypertension may underpin the development of cardiovascular events. In the present study, we evaluated the effects of weight loss (WL) on renal function, especially focusing on sympathetic nervous activity. In 154 overweight or obese Japanese men (89 normotensive and 65 untreated mild hypertensive subjects), body weight, body mass index (BMI), total body fat mass, blood pressure (BP), serum creatinine, blood urea nitrogen, creatinine clearance (CCr) (calculated with the Cockcroft-Gault equation) and plasma norepinephrine (NE) were measured before and after a 12-month period of WL with a mild caloric-restricted diet and exercise. A significant WL was defined as 10% or more WL compared with the entry period. In total, 97 (63.0%) subjects succeeded in significant (by 14.3%) WL at 12 months, and 57 subjects (37.0%) did not succeed in significant WL but they lost 7.7% weight. At entry, levels of plasma NE, serum creatinine and fat mass were significantly lower and CCr was greater in the group with a significant WL compared with those without WL. BMI, total body fat mass and plasma NE significantly decreased, and CCr increased with WL. At both baseline and at the 12-month period, fat mass and plasma NE negatively correlated with CCr and positively correlated with creatinine at each time point. Changes in fat mass and plasma NE over 12 months correlated with changes in creatinine, and only changes in fat mass negatively correlated with changes in CCr. Basal fat mass and plasma NE correlated positively with serum creatinine at 12 months and negatively with CCr at the same time point. In multiple regression analyses, basal plasma NE and fat mass were significant determinants of serum creatinine levels and CCr at 12 months.In conclusion, WL improved renal function (as evident from measures of creatinine and CCr) in overweight individuals. Basal plasma NE levels and total body fat mass could be predictors for improvement in renal function associated with WL. Suppression of sympathetic nervous activation associated with WL may have a role in the ameliorative effects on renal function.

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“…Various other molecules, such as circulating levels of visfatin, leptin, resistin, and aldosterone have been reported to be increased both in patients with CKD [50,51,[60][61][62] and in those with NAFLD/NASH [63][64][65][66]. Recently, some investigators have also measured circulating levels of advanced glycation endproducts (AGE) and its soluble receptors (s-RAGE) in patients with CKD and in those with NAFLD/NASH [67][68][69][70].…”

Section: Increased Incidence Of Chronic Kidney Disease In Patients Wimentioning

confidence: 95%

Risk of chronic kidney disease in patients with non-alcoholic fatty liver disease: Is there a link?

Targher

Chonchol

Zoppini

et al. 2011

Journal of Hepatology

166

131

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Non-alcoholic fatty liver disease (NAFLD) has emerged as a growing public health problem worldwide. Increasing recognition of the importance of NAFLD and its association with the features of the metabolic syndrome has stimulated an interest in its putative role in the development and progression of chronic kidney disease (CKD). Accumulating evidence suggests that NAFLD and CKD share many important cardio-metabolic risk factors and common pathogenetic mechanisms and that NAFLD is associated with an increased prevalence and incidence of CKD. This association appears to be independent of obesity, hypertension, and other potentially confounding factors, and it occurs both in patients without diabetes and in those with diabetes. Although further research is needed to establish a definitive conclusion, these observations raise the possibility that NAFLD is not only a marker of CKD but also might play a part in the pathogenesis of CKD, possibly through the systemic release of several pro-inflammatory/pro-coagulant mediators from the steatotic/inflamed liver or through the contribution of NAFLD itself to insulin resistance and atherogenic dyslipidemia. However, given the heterogeneity and small number of observational longitudinal studies, further research is urgently required to corroborate the prognostic significance of NAFLD for the incidence of CKD, and to further elucidate the complex and intertwined mechanisms that link NAFLD and CKD. If confirmed in future large-scale prospective studies, the potential adverse impact of NAFLD on kidney disease progression will deserve particular attention, especially with respect to the implications for screening and surveillance strategies in the growing number of patients with NAFLD.

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Obesity hypertension: the emerging role of leptin in renal and cardiovascular dyshomeostasis

Cited by 22 publications

References 79 publications

No Association Between Leptin Levels and Sleep Duration or Quality in Obese Adults

No Association Between Leptin Levels and Sleep Duration or Quality in Obese Adults

Effects of weight loss on renal function in overweight Japanese men

Risk of chronic kidney disease in patients with non-alcoholic fatty liver disease: Is there a link?

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