Abstract
The expression profiles of adiponectin, resistin, 5′-AMP-activated protein kinase α (AMPKα), hypoxia-inducible factor-1α (HIF-1α), and key enzymes of glucose and fatty acid metabolism and oxidative phosphorylation in rat retroperitoneal white adipose tissue (RpWAT) during 45-day cold acclimation were examined. After transient suppression on day 1, adiponectin protein level increased following sustained cold exposure. In parallel, on day 1, the protein level of HIF-1α was strongly induced and AMPKα suppressed, while afterwards the reverse was seen. What is more, after an initial decrease on day 1, a sequential increase in pyruvate dehydrogenase, acyl-CoA dehydrogenase, cytochrome c oxidase, and ATP synthase and a decrease in acetyl-CoA carboxylase (from day 3) were observed. Similar to adiponectin, protein level of resistin showed a biphasic profile: it increased after days 1, 3, and 7 and decreased below the control after 21 days of cold-acclimation. In summary, the data suggest that adiponectin and resistin are important integrators of RpWAT metabolic response and roles it plays during cold acclimation. It seems that AMPKα mediate adiponectin effects on metabolic remodeling RpWAT during cold acclimation.
Highlights
Acclimation to low temperature induces profound shifts in energy expenditure aimed at maintaining a stable body temperature [1]
The observed inverse expression profile of HIF-1α and phospho-AMPKα on cold exposure strongly suggests that the interplay between these molecules integrates adiponectin level and metabolic remodeling of retroperitoneal white adipose tissue (RpWAT) from dormant tissue to tissue with higher oxidative capacity
On day 1 of cold exposure, the HIF-1α protein level increased in parallel with a decrease in the level of adiponectin, phospho-AMPKα, and important enzymes indicative of oxidative metabolism (PDH, ACADM, ATP synthase, and cytochrome c oxidase), while the reverse was seen after 1 day of cold exposure; the normalization of hypoxia-inducible factor-1α (HIF1α) was coupled with an increase in adiponectin, activation of AMPKα, and all the above-mentioned metabolic enzymes
Summary
Acclimation to low temperature induces profound shifts in energy expenditure aimed at maintaining a stable body temperature [1]. More recent developments in adipose tissue research have shown that WAT integrates metabolic signals and rapidly responds to changing environments by synthesizing endocrine factors adipokines. These factors initiate powerful feedback actions at the systemic level involved in the regulation of food intake and energy expenditure, that is, metabolic homeostasis. What is more, these factors exert local paracrine and autocrine actions, strongly affecting the metabolic response of WAT and its metabolic role in different metabolic states [12]
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