Long-term impact of vertical banded gastroplasty (VBG) on plasma concentration of leptin, soluble leptin receptor, ghrelin, omentin-1, obestatin, and retinol binding protein 4 (RBP4) in patients with severe obesity

Siejka, Agnieszka; Jankiewicz-Wika, Joanna; Kołomecki, Krzysztof; Cywiński, Jacek B.; Piestrzeniewicz, Katarzyna; Świętosławski, Jacek; Stępień, H; Komorowski, Jan

doi:10.1016/j.cyto.2013.07.026

Cited by 28 publications

(20 citation statements)

References 12 publications

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“…We confirmed the inverse association between serum omentin and BMI, but extended previous studies by the observation that this association was largely due to lipid levels and adiponectin. The aforementioned study on bariatric surgery corroborates the notion that omentin and BMI may not be causally related because a 17% reduction in BMI corresponding to a weight loss of 22.8 kg was not associated with any change in omentin during the first 3 months of follow-up (30).…”

Section: Omentin and Bmisupporting

confidence: 69%

“…Both the hypocaloric diet study and the exercise study reported significant increases in omentin, which associated with an improvement of HOMA-IR, but these interventions also decreased LDL cholesterol and triglyceride levels (13,29). Bariatric surgery induced a substantial weight loss and a decrease in HOMA-IR within 3 months (means at baseline and after 3 months 3.6 and 1.4), but no notable change in plasma omentin levels (30). Interestingly, the levels of total, LDL and HDL cholesterol as well as triglyceride levels remained also unchanged during these 3 months.…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

“…Among these studies, one did not observe a significant association in an Amish population (7), whereas the two others found inverse associations in Chinese samples (12,14), but their multivariate models did not consider lipid levels or adiponectin as potential mediators. In this context, three small intervention studies are of interest, which examined the association between changes in omentin and HOMA-IR in overweight/obese individuals resulting from weight loss following a hypocaloric diet for 4 months (29), aerobic exercise for 3 months (13) or bariatric surgery (30). Both the hypocaloric diet study and the exercise study reported significant increases in omentin, which associated with an improvement of HOMA-IR, but these interventions also decreased LDL cholesterol and triglyceride levels (13,29).…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

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Adiponectin may mediate the association between omentin, circulating lipids and insulin sensitivity: results from the KORA F4 study

Herder

Ouwens

Carstensen

et al. 2015

European Journal of Endocrinology

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Objective: Reduced circulating omentin levels have been reported in obesity and type 2 diabetes, but data were mostly derived from univariate analyses in small study samples. This study aimed to investigate the relationship between omentin, abnormal glucose tolerance and related metabolic factors in a large population-based cross-sectional study. Design and methods: Serum omentin was measured by ELISA in 1092 participants of the German KORA F4 survey (2006)(2007)(2008). Associations between omentin serum levels, glucose tolerance (assessed with an oral glucose tolerance test) and diabetesrelated factors were estimated using logistic and linear regression models respectively. Results: Serum levels of omentin were not related to categories of glucose tolerance. However, serum omentin was positively associated with whole-body insulin sensitivity index (ISI (composite)) and HDL cholesterol and showed inverse associations with 2-h post-load glucose, fasting insulin, homeostasis model assessment-estimated insulin resistance, BMI and triglycerides (all P%0.03 after adjustment for age, sex and lifestyle factors). Further adjustment for BMI and/or serum lipids attenuated the associations with parameters of glucose metabolism, whereas adjustment for serum adiponectin virtually abolished all aforementioned associations. In contrast, adjustment for omentin had no effect on the positive association between adiponectin levels and ISI (composite). Conclusions: The data from this large population-based cohort show that circulating omentin levels are associated with insulin sensitivity. Our observations further suggest that omentin acts via upregulation of adiponectin, which in turn affects lipid metabolism and thereby also indirectly enhances insulin sensitivity, but mechanistic studies are required to corroborate this hypothesis.

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Section: Omentin and Bmisupporting

confidence: 69%

Section: European Journal Of Endocrinologymentioning

confidence: 99%

Section: European Journal Of Endocrinologymentioning

confidence: 99%

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Adiponectin may mediate the association between omentin, circulating lipids and insulin sensitivity: results from the KORA F4 study

Herder

Ouwens

Carstensen

et al. 2015

European Journal of Endocrinology

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“…In agreement, liver-specific insulin receptor knockout (LIRKO) mice displays markedly increased sOBR levels in circulation and enhanced leptin sensitivity (Cohen et al 2007). Moreover, obese subjects after weight loss surgery (Laimer et al 2002, Siejka et al 2013, diet therapy (Wolfe et al 2004, Gajewska et al 2013 or physical training (Balagopal et al 2010, Gajewska et al 2013) demonstrated increased sOBR levels, indicating the restoration in leptin sensitivity. Taken together, these studies implicate that manipulating sOBR levels may provide a therapeutic approach for rescue of leptin sensitivity.…”

Section: Introductionmentioning

confidence: 68%

Metformin increases hepatic leptin receptor and decreases steatosis in mice

Tang

Xiang

et al. 2016

Journal of Endocrinology

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In addition to the ascertained efficacy as antidiabetic drug, metformin is increasingly being used as weight-loss agent in obesity, and as insulin sensitizer in nonalcoholic fatty liver disease (NAFLD). However, the mechanisms underlying these effects are still incompletely understood. Emerging evidence suggest metformin as leptin sensitizer to mediate the weight-loss effect in the brain. In this study, we investigated effects of metformin on expression of leptin receptors in liver and kidney in mice. C57BL/6 mice were fed with chow diet (CD) or high-fat diet (HF) for 5 months. Afterward, mice were treated with metformin (50 mg/kg or 200 mg/kg) for 15 days. Metabolic parameters and hepatic gene expression were analyzed at the end of the treatment. We also tested the effects of metformin on plasma-soluble leptin receptor (sOB-R) levels in newly diagnosed type 2 diabetes mellitus (T2DM) patients, and assessed its effect on hepatosteatosis in mice. Results showed that metformin upregulates the expression of leptin receptors (OB-Ra, -Rb, -Rc, and -Rd) in liver but not kidney. The stimulation effect is dosedependent in both chow and HF mice. Upregulation of OB-Rb, long signaling isoform, needs a relatively higher dose of metformin. This effect was paralleled by increased sOBR levels in mice and T2DM patients, and decreased hepatic triglyceride (TG) content and lipogenic gene expression, including sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthase (FAS) and acetyl-CoA carboxylase-1 (ACC-1). Taken together, these data identify hepatic leptin receptor as target gene being upregulated by metformin which may enhance leptin sensitivity in liver to alleviate steatosis.

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“…Thus, some have shown decreased concentrations of obestatin in the blood of patients with insulin resistance (16), obesity (24), or type 2 diabetes (25); similarly, studies have reported increased plasma levels of obestatin after weight reduction achieved by bariatric surgery in patients with obesity (26) or type 2 diabetes (27), supporting the notion of an inverse relationship between circulating obestatin and body weight. This view, however, has been undermined by the results of other studies demonstrating that obestatin plasma levels are increased in patients with obesity (28) or metabolic syndrome (29) and unchanged after weight loss induced by gastric surgery (30,31). The precise reasons for these discrepancies are unknown, but in addition to possible differences in the characteristics of the patients studied, variations in the specificity of the methods used for detection of obestatin compared with prepro-ghrelin (32) are another likely contributor.…”

Section: Discussionmentioning

confidence: 68%

Vascular Effects of Obestatin in Lean and Obese Subjects

Schinzari

Veneziani

et al. 2017

Diabetes

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Obese patients have impaired vasodilator reactivity and increased endothelin 1 (ET-1)-mediated vasoconstriction, two abnormalities contributing to vascular dysfunction. Obestatin, a product of the ghrelin gene, in addition to favorable effects on glucose and lipid metabolism, has shown nitric oxide (NO)-dependent vasodilator properties in experimental models. Given these premises, we compared the effects of exogenous obestatin on forearm flow in lean and obese subjects and assessed its influence on ET-1-dependent vasoconstrictor tone in obesity. In both lean and obese participants, infusion of escalating doses of obestatin resulted in a progressive increase in blood flow from baseline (both P < 0.001). This vasodilation was predominantly mediated by enhanced NO activity, because N G -monomethyl-L-arginine markedly blunted the flow response to obestatin in both groups (both P < 0.05 vs. saline). In obese subjects, antagonism of ET A receptors by BQ-123 increased forearm flow during saline (P < 0.001) but did not induce additional vasodilation (P > 0.05) during obestatin. Circulating obestatin levels were not different between lean and obese participants (P = 0.41). Our findings indicate that obestatin causes NO-dependent vasodilation in the human circulation. This effect is preserved in obesity, where it is accompanied by reduced ET-1-mediated vasoconstriction. These latter observations make obestatin a promising target for vascular prevention in obesity and diabetes.According to the current figures of the World Health Organization, the worldwide prevalence of obesity is still on the rise, carrying an increased burden of type 2 diabetes and other untoward consequences, especially cardiovascular complications. Impaired vasodilator reactivity has been recognized as an early hemodynamic abnormality characteristic of these patients (1), but also increased vasoconstrictor tone, predominantly resulting from enhanced endothelin (ET)-1 activity (2,3), has been shown to importantly contribute to their vascular dysfunction and damage.Obestatin was identified in 2005 as a ghrelin-associated peptide derived from alternative splicing of the common precursor prepro-ghrelin and was originally reported to reduce food intake and gastric emptying through activation of the G-protein-coupled receptor (GPCR) GPR39 (4). Even though these effects on feeding behavior and gastrointestinal motion have been subsequently disputed and the precise identity of its cognate receptor(s) is still a matter of debate (5), obestatin indisputably exerts a variety of effects in different cell types, including pancreatic b-cells, where it increases survival and proliferation by inhibiting apoptosis and inflammation (6,7). In line with these actions, other favorable effects of obestatin have been observed on glucose and lipid metabolism, such as increased glucose uptake and insulin sensitivity as well as inhibition of lipolysis in human adipocytes (7,8).Interestingly, in addition to its helpful metabolic properties, obestatin has been shown to provide va...

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Long-term impact of vertical banded gastroplasty (VBG) on plasma concentration of leptin, soluble leptin receptor, ghrelin, omentin-1, obestatin, and retinol binding protein 4 (RBP4) in patients with severe obesity

Cited by 28 publications

References 12 publications

Adiponectin may mediate the association between omentin, circulating lipids and insulin sensitivity: results from the KORA F4 study

Adiponectin may mediate the association between omentin, circulating lipids and insulin sensitivity: results from the KORA F4 study

Metformin increases hepatic leptin receptor and decreases steatosis in mice

Vascular Effects of Obestatin in Lean and Obese Subjects

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