Adipose Tissue Dysfunction in Nascent Metabolic Syndrome

Abstract

The metabolic syndrome (MetS) confers an increased risk for both type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Moreover, studies on adipose tissue biology in nascent MetS uncomplicated by T2DM and/or CVD are scanty. Recently, we demonstrated that adipose tissue dysregulation and aberrant adipokine secretion contribute towards the syndrome's low-grade chronic proinflammatory state and insulin resistance. Specifically, we have made the novel observation that subcutaneous adipose tissue (SAT) in subjects with nascent MetS has increased macrophage recruitment with cardinal crown-like structures. We have also shown that subjects with nascent MetS have increased the levels of SAT-secreted adipokines (IL-1, IL-6, IL-8, leptin, RBP-4, CRP, SAA, PAI-1, MCP-1, and chemerin) and plasma adipokines (IL-1, IL-6, leptin, RBP-4, CRP, SAA, and chemerin), as well as decreased levels of plasma adiponectin and both plasma and SAT omentin-1. The majority of these abnormalities persisted following correction for increased adiposity. Our data, as well as data from other investigators, thus, highlight the importance of subcutaneous adipose tissue dysfunction in subjects with MetS and its contribution to the proinflammatory state and insulin resistance. This adipokine profile may contribute to increased insulin resistance and low-grade inflammation, promoting the increased risk of T2DM and CVD.

Role of omentin and vaspin in metabolic diseases in association with psoriasis

“…Positive correlations have been found with the concentration of HDL cholesterol and plasma adiponectin [20]. Interesting findings have been reported by Bremer et al, including a reduced concentration of omentin in the serum and subcutaneous adipose tissue in patients with metabolic syndrome (MS) in relation to the control group, regardless of obesity [21]. Omentin increases insulin sensitivity by stimulating insulin-dependent glucose uptake in subcutaneous and visceral adipose tissue cells, muscles and liver [5].…”

“…Interesujące spostrzeżenia przedstawili Bremer i wsp. -stwierdzili zmniejszone stężenie omentyny w surowicy i podskórnej tkance tłuszczowej u osób z zespołem metabolicznym (ZM) w porównaniu z grupą kontrolną, niezależnie od otyłości [21]. Omentyna zwiększa insulinowrażliwość poprzez stymulację insulinozależnego wychwytu glukozy w komórkach tłusz-czowych tkanki podskórnej i trzewnej, w mięśniach i wątrobie [5].…”

Body composition indices of a load–capacity model: gender- and BMI-specific reference curves

“…Metabolic load is assumed to emerge through the life course. In adults, high levels of adiposity, sedentary behaviour and lipogenic diet all exacerbate metabolic load (22,23) . This approach can be adapted to SO by treating lean mass, in particular skeletal muscle mass, as a dimension of metabolic capacity especially relevant for physical activity, with further implications for fuel utilisation.…”

Вплив нутрiєнтної корекцiї на рiвень адипонектину в циркуляцiї та фактори кардiоваскулярного ризику у хворих на цукровий дiабет 2-го типу з неалкогольною жировою хворобою печінки

“…Також адипонектину притаманна ангiопротек-тивна дiя (зниження експресiї молекул мiжклiтинної адгезiї та пригнiчення пролiферацiї мiоцитiв судин-ною стiнкою [37][38][39]; зниження системної запаль-ної реакцiї, сприяння процесу активацiї репарацiї клiтин) [40]. Тепер активно дискутуються питання щодо генетичної детермiнацiї розвитку НАЖХП, а саме ролi однонуклеотидного полiморфiзму гена адипонектину [41][42][43][44].…”