Adipokines – removing road blocks to obesity and diabetes therapy

Abstract

Prevention of obesity and therapeutic weight loss interventions have provided only limited long term success. Therefore there is an urgent need to develop novel pharmacological treatment strategies, which target mechanisms underlying positive energy balance, excessive fat accumulation and adverse fat distribution. Adipokines may have potential for future pharmacological treatment strategies of obesity and metabolic diseases, because they are involved in the regulation of appetite and satiety, energy expenditure, endothelial function, blood pressure, insulin sensitivity, adipogenesis, fat distribution and insulin secretion and others. There are important road blocks on the way from an adipokine candidate to the clinical use a therapeutic compound. Such road blocks include an incomplete understanding of the mechanism of action, resistance to a specific adipokine, side effects of the adipokine and others. This review focuses on the potential of selected adipokines as therapeutic tools or targets and discusses important road blocks, which currently prevent their clinical use.

Acarbose versus trans-chalcone: comparing the effect of two glycosidase inhibitors on obese mice

“…Levels of the adipokines leptin and adiponectin, which are considered to be therapeutic targets/tools in obesity (24), were also observed to be affected by these compounds. In our study, acarbose was found to increase adiponectin levels in the treated obese rats, which is in accordance with previous reports concerning diabetic patients (25) and diabetic obese rats (26).…”

Critically Discuss the Revival of Leptin for Obesity Therapy

“…However, in recent years researchers have demonstrated that a multi-therapy of leptin in combination with other leptin sensitisers may be able to improve peripheral leptin sensitivity and may hold therapeutic promise (Moon et al, 2011;Müller et al, 2012;Matthias, 2014;Crujeiras et al, 2015;Park & Ahima, 2015). These leptin sensitisers target distinct neuroendocrine systems related to leptin signalling pathology.…”

“…Nevertheless, overcoming resistance to the leptin therapy continues to challenge the researchers. In recent years some preclinical studies have surprisingly demonstrated that resistance to leptin can be reversed and the effects of leptin therapy can be amplified by several leptin sensitisers (Moon et al, 2011;Müller et al, 2012;Matthias, 2014;Crujeiras et al, 2015;Park & Ahima, 2015). Accordingly, it is the aim of this paper to critically discuss the plausible revival of leptin for obesity therapy with reference to research findings on various influencing factors contributing to the level of expression and secretion of leptin.…”

Asociación de la resistina con variables de dimensión y composición corporal en eutróficos y obesos

“…El exceso o déficit del TA resultará en una producción o liberación alterada de los mediadores antes mencionados, ocasionando una comunicación defectuosa con otros órganos, alteraciones en el metabolismo y el desarrollo posterior de enfermedades endocrino-metabólicas. Un exceso de TA en la región visceral se ha asociado con insulino resistina, variables de dimensión y composición corporal -A. souki et al rev Med chile 2016; 144: 307-316 resistencia (IR), DM2, dislipidemia, hiperglicemia e hipertensión, así como estados protrombóticos y proinflamatorios [4][5][6] .…”