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. 1. Introduction Acclimation to low temperature induces profound shifts in energy expenditure aimed at maintaining a stable body temperature [1]. Many aspects of adaptive metabolic changes in muscles, brown adipose tissue, and liver as the sites of thermoregulatory thermogenesis, that is, tissues with the highest oxygen consumption, have been the subject of considerable research [2–7]. By contrast, the data related to white adipose tissue (WAT) during cold acclimation are mainly focused on the metabolic pathways of the synthesis and breakdown of triglycerides, as ways of controlling fatty acids release, for example, availability for other tissues [8, 9], as well as on the morphological plasticity—the appearance of multilocular, brown fat-like cells [10, 11]. It is known that the response of white fat tissue in the conditions of increased whole body energy demands involves complex recruitment in WAT at the metabolic and endocrine levels. 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
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