Increased Resistin Gene and Protein Expression in Human Abdominal Adipose Tissue

Abstract

Resistin, a novel signalling molecule isolated in mice has been suggested to be the putative hormone thought to link obesity with type 2 diabetes. The aim of this study was to examine resistin protein expression in human adipose tissue depots and resistin secretion in isolated adipose cells, to characterize resistin expression in human adipose tissue. Both resistin mRNA and protein expression were analysed from human adipose tissue (n = 5 adipose tissue samples: abdominal subcutaneous (Sc) n = 19, abdominal omental adipose tissue (Om) n = 10, thigh n = 9, breast n = 7). Resistin protein expression levels were similar in both the abdominal Sc and Om adipose tissue depots, and expression in abdominal fat depots were increased compared with thigh (p < 0.001) and breast tissue depots (p < 0.001). These findings were consistent with the mRNA expression studies. Resistin was secreted from both pre-adipocytes and adipocytes cells. Thus, resistin resides within isolated adipose cells and is expressed and secreted in human adipose tissue. In conclusion, this study confirms the expression of resistin in human adipose tissue and increased expression in abdominal fat, this suggests a potential role in linking central obesity to type 2 diabetes and/or cardiovascular disease.

Mouse and Human Resistins Impair Glucose Transport in Primary Mouse Cardiomyocytes, and Oligomerization Is Required for This Biological Action

“…Resistin is secreted from primary adipocytes isolated from subcutaneous and omental adipose tissue depots in humans, and the expression is 4-fold higher in abdominal adipose tissue versus adipose tissue obtained from the thigh (13,14). Whether or not these regional differences in resistin expression contribute to the association between visceral obesity and insulin resistance is not known.…”

Visceral obesity and cardiometabolic risk: features of hormonal and immune regulation

“…Висцеральное ожирение ассоциируется с форми-рованием аномального метаболического профиля пациентов, что обусловлено нарушением обменных процессов в ВЖТ, ее патологической гормональной активностью, выраженной васкуляризацией, а также более высокой, в сравнении с ПЖТ, плотностью липо-литических бета-адренорецепторов, глюкокортикоид-ных и андрогенных рецепторов [9,10].…”

Role of lipocytocins in the pathogenesis of metabolic syndrome

“…Ðåçèñòèí, ùî ñåêðåòóºòüñÿ àäèïîöèòàìè é ìîíîöèòàìè, òàêîae ÿê ×ÍÏ ³ ²Ë-6, ìຠïðîçà-ïàëüí³ âëàñòèâîñò³ [67]. Ðåçèñòèí âïëèâຠíà aeèðîâèé îáì³í çà ïðèíöèïîì çâîðîòíîãî çâ'ÿç-êó: ç îäíîãî áîêó, éîãî êîíöåíòðàö³ÿ ï³äâè-ùóºòüñÿ ç äèôåðåíö³þâàííÿì àäèïîöèò³â, ç ³í-øîãî -ðåçèñòèí ïðèãí³÷óº àäèïîãåíåç [91].…”