Long-term Changes in Leptin, Chemerin and Ghrelin Levels Following Different Bariatric Surgery Procedures: Roux-en-Y Gastric Bypass and Sleeve Gastrectomy

Terra, Ximena; Auguet, Teresa; Guiu‐Jurado, Esther; Berlanga, Alba; Orellana-Gavaldà, Josep Maria; Hernández, Mercè; Sabench, Fàtima; Porras, José Antonio; Llutart, Jordi; Martínez, Salomé; Aguilar, Carmen; Déjardin, Daniel del Castillo; Richart, C

doi:10.1007/s11695-013-1033-9

Cited by 103 publications

(58 citation statements)

References 32 publications

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“…More recently, infusion of chemerin into the mouse modestly elevated blood pressure (20), and chemerin has been suggested to reduce nitric oxide signaling in the rat aorta (29). Understanding the functions of chemerin is important, because circulating levels of chemerin can be reduced and health can be improved through a number of interventions that include bariatric surgery and exercise (7,22,24,28,30,34,39,44). Other pathologies, such as arterial stiffness (54) syndrome (15,18), have been associated with elevated chemerin levels.…”

Section: Discussionmentioning

confidence: 99%

The adipokine chemerin amplifies electrical field-stimulated contraction in the isolated rat superior mesenteric artery

Darios

Winner

Charvat

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Darios ES, Winner BM, Charvat T, Krasinksi A, Punna S, Watts SW. The adipokine chemerin amplifies electrical field-stimulated contraction in the isolated rat superior mesenteric artery. Am J Physiol Heart Circ Physiol 311: H498 -H507, 2016. First published July 1, 2016; doi:10.1152/ajpheart.00998.2015.-The adipokine chemerin causes arterial contraction and is implicated in blood pressure regulation, especially in obese subjects with elevated levels of circulating chemerin. Because chemerin is expressed in the perivascular adipose tissue (PVAT) that surrounds the sympathetic innervation of the blood vessel, we tested the hypothesis that chemerin (endogenous and exogenous) amplifies the sympathetic nervous system in mediating electrical field-stimulated (EFS) contraction. The superior mesenteric artery, with or without PVAT and with endothelium and sympathetic nerve intact, was mounted into isolated tissue baths and used for isometric contraction and stimulation. Immunohistochemistry validated a robust expression of chemerin in the PVAT surrounding the superior mesenteric artery. EFS (0.3-20 Hz) caused a frequency-dependent contraction in isolated arteries that was reduced by the chemerin receptor ChemR23 antagonist CCX832 alone (100 nM; with, but not without, PVAT), but not by the inactive congener CCX826 (100 nM). Exogenous chemerin-9 (1 M)-amplified EFSinduced contraction in arteries (with and without PVAT) was blocked by CCX832 and the ␣-adrenergic receptor antagonist prazosin. CCX832 did not directly inhibit, nor did chemerin directly amplify, norepinephrine-induced contraction. Whole mount immunohistochemical experiments support colocalization of ChemR23 with the sympathetic nerve marker tyrosine hydroxylase in superior mesenteric PVAT and, to a lesser extent, in arteries and veins. These studies support the idea that exogenous chemerin modifies sympathetic nervemediated contraction through ChemR23 and that ChemR23 may be endogenously activated. This is significant because of the wellappreciated role of the sympathetic nervous system in blood pressure control. BECAUSE OF ITS LOCATION, the perivascular adipose tissue (PVAT) has the potential to affect the function of the blood vessels it encases. This can occur by secretion of adipokines that directly affect vascular tone, such as the relaxant adiponectin (25). We recently discovered the protein chemerin in PVAT and demonstrated that a shorter chemerin agonist, chemerin-9, caused direct arterial contraction through activation of the best-characterized chemerin receptor, ChemR23 (3,8,27,33,38,48). Chemerin is secreted from the liver and fat depots (10), functioning as an adipokine that regulates adipogenesis (12,31,32) and as an activator of inflammatory cells (13,50,52). Circulating levels of chemerin are positively associated with body mass index (1,4,9,16,36,37,40). Because of our long-term interest in understanding whether chemerin could play a role in obesity-associated hypertension, we turned our attention to a means by which arterial function could be m...

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Section: Discussionmentioning

confidence: 99%

The adipokine chemerin amplifies electrical field-stimulated contraction in the isolated rat superior mesenteric artery

Darios

Winner

Charvat

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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“…Chemerin acts locally on adipocytes, inducing adipogenesis and lipolysis, but it is also secreted to the bloodstream, promoting insulin resistance in skeletal muscle (105,272,288). Obesity and metabolic syndrome are associated with increased circulating levels of chemerin, which are significantly decreased after weight loss induced by bariatric surgery (27,35,69,315). A higher gene expression of chemerin and its receptor CMKLR1 has been also found in the visceral adipose tissue of obese patients (27,35).…”

Section: Recruitment Of Proinflammatory Immune Cells In Obesity Perpementioning

confidence: 99%

Revisiting the adipocyte: a model for integration of cytokine signaling in the regulation of energy metabolism

Rodrı́guez

Ezquerro

Méndez‐Giménez

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

234

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Adipose tissue constitutes an extremely active endocrine organ with a network of signaling pathways enabling the organism to adapt to a wide range of different metabolic challenges, such as starvation, stress, infection, and short periods of gross energy excess. The functional pleiotropism of adipose tissue relies on its ability to synthesize and release a huge variety of hormones, cytokines, complement and growth factors, extracellular matrix proteins, and vasoactive factors, collectively termed adipokines. Obesity is associated with adipose tissue dysfunction leading to the onset of several pathologies including type 2 diabetes, dyslipidemia, nonalcoholic fatty liver, or hypertension, among others. The mechanisms underlying the development of obesity and its associated comorbidities include the hypertrophy and/or hyperplasia of adipocytes, adipose tissue inflammation, impaired extracellular matrix remodeling, and fibrosis together with an altered secretion of adipokines. Recently, the potential role of brown and beige adipose tissue in the protection against obesity has been also recognized. In contrast to white adipocytes, which store energy in the form of fat, brown and beige fat cells display energy-dissipating capacity through the promotion of triacylglycerol clearance, glucose disposal, and generation of heat for thermogenesis. Identification of the morphological and molecular changes in white, beige, and brown adipose tissue during weight gain is of utmost relevance for the identification of pharmacological targets for the treatment of obesity and its associated metabolic diseases. white and brown adipogenesis; fat browning; adipocyte hypertrophy and hyperplasia; adipose tissue inflammation; extracellular matrix remodeling THE ADIPOSE ORGAN REPRESENTS a special loose connective tissue containing adipocytes and several cell types surrounded by capillary and innervation networks (47, 79, 82). Adipocytes comprise ϳ35-70% of adipose mass, and the other cell types found in the stroma-vascular fraction include preadipocytes, mesenchymal stem cells, macrophages and other immune cells, and endothelial and smooth muscle cells, among others (79). The classical functions of adipose tissue are the storage of energy in the form of triacylglycerols (TG) and as thermal insulator. Adipocytes were formerly classified into two main types: white adipocytes, which store energy in the form of fat, and brown adipocytes, which induce thermogenesis (82). The current classification scheme includes a third category of adipocytes, termed beige or brite (brown-in-white) adipocytes, which can be considered inducible brown-like cells with thermogenic properties (340). Since the identification of leptin in 1994 (359), adipose tissue has emerged as an extremely active endocrine organ that secretes a huge variety of hormones, cytokines, growth factors, and vasoactive factors that are collectively termed adipokines (67, 81,235,262). Over the last three decades, overwhelming evidence has proven that adipokines not only influence adipobiol...

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“…48 Furthermore, bariatric surgery has also been shown to impact several adipocytokines 49 while declining leptin levels were observed following bariatric surgery. [50][51][52][53] Of note, a recent analysis of early hormone changes following bariatric surgery found a decrease of ghrelin, leptin and gastrin as soon as two weeks after surgery. These data are remarkable, since changes of the adipocytokine profile seem to precede weight loss.…”

Section: Immunological Consequences Of Bariatric Surgerymentioning

confidence: 99%

Obesity-related immune responses and their impact on surgical outcomes

et al. 2015

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The obesity epidemic represents a critical disease burden with broad clinical consequences. At the same time, obesity has been linked to inferior surgical outcomes and considered a contraindication for some elective surgical procedures. A growing body of mechanistic evidence has accumulated linking obesity to changes of metabolism and immune responses. This concept provides an integrated inflammatory network based on the perception of obesity as a state of chronic low-grade inflammation. With a more detailed understanding of this dynamic network and mechanistic insights, novel treatment and management strategies may be developed with the goal to optimize surgical outcomes in obese patients.

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Long-term Changes in Leptin, Chemerin and Ghrelin Levels Following Different Bariatric Surgery Procedures: Roux-en-Y Gastric Bypass and Sleeve Gastrectomy

Cited by 103 publications

References 32 publications

The adipokine chemerin amplifies electrical field-stimulated contraction in the isolated rat superior mesenteric artery

The adipokine chemerin amplifies electrical field-stimulated contraction in the isolated rat superior mesenteric artery

Revisiting the adipocyte: a model for integration of cytokine signaling in the regulation of energy metabolism

Obesity-related immune responses and their impact on surgical outcomes

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