Physiological, pathological and potential therapeutic roles of adipokines

Falcão-Pires, Inês; Castro-Chaves, Paulo; Miranda-Silva, Daniela; Lourenço, André P.; Leite‐Moreira, Adelino F.

doi:10.1016/j.drudis.2012.04.007

Cited by 120 publications

(107 citation statements)

References 156 publications

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“…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 adipobiology and function in an autocrine/paracrine manner but also are released to the bloodstream to regulate numerous biological processes in an endocrine fashion (Table 1).…”

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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

235

186

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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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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

235

186

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“…Dose, method of administration, experimental subject, could contribute to this variation. It is suggested that apelin, reported the effects on cardiovascular regulation, can be a potential therapeutic target in hypertension (36). Nesfatin-1, secreted in hypothalamus and brain stem, has been reported to be a peptide effi cacy in the control of appetite (anorexigenic effects) regardless of leptin pathway (16,11).…”

Section: Discussionmentioning

confidence: 99%

Supplementation of apelin increase plasma levels of nesfatin-1 in normal and DOCA-salt hypertensive rats

Akçılar¹,

Ayada²,

Turgut³

et al. 2015

BLL

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Aims:We aimed to observe the effects of apelin supplementation on the plasma levels of nesfatin-1 in DOCA-salt hypertensive and normal rats. Methods: For this purpose, 28 young Wistar albino male rats were divided into four groups; Control (C), Control + Apelin (C+A), Hypertension (HT) and Hypertension + Apelin (HT+A). Hypertension was induced by injection of DOCA-salt (25 mg/kg, s.c.) twice weekly, 4 weeks, whereas intraperitoneal apelin was administered (200 μg.kg -1 ) for 17 days. Plasma nesfatin-1 and apelin levels were measured with ELISA. Systolic blood pressure was monitored using a tail cuff system. The relationships between plasma nesfatin levels and blood pressure were assessed. Results: Plasma nesfatin-1 levels was found lower in control animals compared to C+A, HT and HT+A groups (p = 0.002, p = 0.026 and p = 0.011, respectively). Systolic blood pressures were similar in the C and C+A groups, but systolic blood pressures of the HT and HT+A groups was found signifi cantly higher than the C and C+A groups. Conclusions: In conclusion, apelin administration induced an increment of nesfatin-1 in normal rats and plasma levels of nesfatin-1 increase in DOCA-salt hypertension rats. But apelin addition in hypertension did not cause an extra increase in nesfatin-1 levels. This is the fi rst report to investigate the effect of apelin administration on plasma nesfatin levels of normal and hypertensive rats (Fig. 2, Ref. 44). Text in PDF www.elis.sk.

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“…One third of human cancers produce apelin, which stimulates tumor growth (15). In experimental studies with mice, increased APJ mRNA has been detected, with APJ expression in all peripheral tissues.…”

Section: Introductionmentioning

confidence: 96%

The role of apelin in the assessment of response to chemotherapyand prognosis in stage 4 nonsmall cell lung cancer

Ermin¹,

Çok²,

Veral³

et al. 2016

Turk J Med Sci

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Background/aim: Prediction of response to chemotherapy and prognosis bears clinical significance in patients with lung cancer. The aim of the study was to examine the association between apelin expression in tumor tissues and overall survival, progression-free survival, chemoresistance, and treatment response in stage 4 nonsmall cell lung cancer (NSCLC) patients undergoing chemotherapy.Materials and methods: A total of 81 patients who received chemotherapy due to a biopsy-documented diagnosis of NSCLC between 2004 and 2011 were retrospectively studied. Bronchoscopic biopsy samples were examined immunohistochemically.Results: Of the overall study population (n = 81), the mean age was 59.0 ± 9.2 years; 83% (n = 67) were male and 17% (n = 14) were female. All patients received chemotherapy. A total of 30 patients (37%) had no apelin positivity, while 21 (30%) had 1 +, 20 (25%) had 2 +, and 10 (12%) had 3 + apelin positivity. We detected no association between apelin positivity and overall survival, 6-month survival, or 1-year survival rates (P = 0.05, 0.74, and 0.63). Patients with apelin expression as compared to those without it had shorter overall survival (P = 0.05). Conclusion:Our results suggest that apelin, an angiogenic factor, does not seem to provide significant prognostic information in this patient group.

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Physiological, pathological and potential therapeutic roles of adipokines

Cited by 120 publications

References 156 publications

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

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

Supplementation of apelin increase plasma levels of nesfatin-1 in normal and DOCA-salt hypertensive rats

The role of apelin in the assessment of response to chemotherapyand prognosis in stage 4 nonsmall cell lung cancer

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