Cross-talk between adipose tissue and vasculature: role of adiponectin

Abstract

Adipose tissue is a highly dynamic endocrine organ, secreting a number of bioactive substances (adipokines) regulating insulin sensitivity, energy metabolism and vascular homeostasis. Dysfunctional adipose tissue is a key mediator that links obesity with insulin resistance, hypertension and cardiovascular disease. Obese adipose tissue is characterized by adipocyte hypertrophy and infiltration of inflammatory macrophages and lymphocytes, leading to the augmented production of pro-inflammatory adipokines and vasoconstrictors that induce endothelial dysfunction and vascular inflammation through their paracrine and endocrine actions. By contrast, the secretion of adiponectin, an adipokine with insulin sensitizing and anti-inflammatory activities, is decreased in obesity and its related pathologies. Emerging evidence suggests that adiponectin is protective against vascular dysfunction induced by obesity and diabetes, through its multiple favourable effects on glucose and lipid metabolism as well as on vascular function. Adiponectin improves insulin sensitivity and metabolic profiles, thus reducing the classical risk factors for cardiovascular disease. Furthermore, adiponectin protects the vasculature through its pleiotropic actions on endothelial cells, endothelial progenitor cells, smooth muscle cells and macrophages. Data from both animal and human investigations demonstrate that adiponectin is an important component of the adipo-vascular axis that mediates the cross-talk between adipose tissue and vasculature. This review highlights recent work on the vascular protective activities of adiponectin and discusses the molecular pathways underlying the vascular actions of this adipokine.

Role of lipocytocins in the pathogenesis of metabolic syndrome

“…Ó ïëàçì³ êðîâ³ àäèïîíåêòèí ì³ñòèòüñÿ ó á³ëü-øèõ ê³ëüêîñòÿõ, í³ae ³íø³ ïðîäóêòè AEÒ, éîãî êîí-öåíòðàö³ÿ ñòàíîâèòü 0,01% çàãàëüíîãî ïóëó á³ë-ê³â ïëàçìè [71]. Ó ae³íîê ó íîðì³ ð³âåíü àäèïî-íåêòèíó, ÿê ³ ëåïòèíó, âèùèé, í³ae ó ÷îëîâ³ê³â, ùî ïîÿñíþþòü îñîáëèâîñòÿìè ðîçïîä³ëó ï³äøê³ð-íî¿ aeèðîâî¿ êë³òêîâèíè [70].…”

“…гâåíü àäèïîíåêòè-íó â ïëàçì³ º â³äíîñíî ñòàá³ëüíèì ïðîòÿãîì äîáè, ç íåçíà÷íèì çíèaeåííÿì ó í³÷í³ ÷àñè òà íàéíèae÷èìè êîíöåíòðàö³ÿìè âðàíö³. Ó íîðì³ ð³-âåíü àäèïîíåêòèíó êîëèâàºòüñÿ â ä³àïàçîí³ 1-20 íã/ìë [71]. Äåÿê³ õàð÷îâ³ ïðîäóêòè, çîêðå-ìà á³ëîê ñî¿, ðèá'ÿ÷èé aeèð, ë³íîëåâà êèñëîòà, çäàòí³ ï³äâèùóâàòè ñåêðåö³þ àäèïîíåêòèíó [72].…”

Adipoparacrinology: an Emerging Field in Biomedical Research

“…However, when EAT is totally absent, as in congenital generalized lipodystrophy, coronary atherosclerosis can still occur, suggesting that a homeostatic presence of adipose tissue is required for coronary artery health. Likewise, the normal amount of PAAT is likely to be important in maintaining the homeostasis of vascular tone and blood pressure, since lipoatrophic mice developed hypertension (14,15). On the other end, excessive accumulation of body fat as in obesity impairs PAAT secretion, despite an increase in the amount of PAAT.…”

“…As indicated above, obese adipose tissue is featured by adipocyte hypertrophy leading to hypoxia (16) and invasion of immune cells (4,5); this results in an increased production of pro-inflammatory adipokines. By contrast, the secretion of adiponectin, an adipokine with anti-inflammatory, insulin sensitizing, vasorelaxing and metabotrophic (favourable effects on glucose and lipid metabolism) activities, is decreased in obesity and related vascular diseases (14,15).…”

“…In recent years, the study of adipobiology has become dominated by an apparently increasing list of adipokines implicated in the control of a wide array of physiological and pathological processes (1,(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) including atherogenesis-related processes such as inflammation and vascular tone (21-27). As indicated above, obese adipose tissue is featured by adipocyte hypertrophy leading to hypoxia (16) and invasion of immune cells (4,5); this results in an increased production of pro-inflammatory adipokines.…”