Fasting regulates the expression of adiponectin receptors in young growing pigs1

Abstract

Adiponectin is an adipocyte-derived hormone that can improve insulin sensitivity. Its functions in regulating glucose utilization and fatty acid metabolism in mammals are mediated by 2 subtypes of adiponectin receptors (AdipoR1 and AdipoR2). This study was conducted to determine the effect of fasting on the expression of adiponectin and its receptors. The expression of adiponectin was not affected in s.c. adipose tissue, but adiponectin expression increased in visceral adipose tissue after fasting. In contrast, expression of both AdipoR mRNA was increased in the liver and s.c. adipose tissue of 24-h-fasted pigs compared with fed pigs, but the mRNA in muscle and visceral adipose tissue was not affected by fasting. A third putative adiponectin receptor, T-cadherin, was cloned and the mRNA expression was determined. T-Cadherin has been recognized to act as a vascular adiponectin receptor in vascular endothelial and smooth muscle cells. Our data showed that the expression of T-cadherin was decreased in the muscle of fasted pigs, suggesting that the expression of T-cadherin can be regulated by feeding status. In summary, in young pigs, adiponectin mRNA was up-regulated by fasting in visceral, but not s.c., adipose tissue, whereas AdipoR1 and AdipoR2 mRNA were increased in s.c., but not visceral, adipose tissue. The adiponectin receptor, T-cadherin, was expressed in s.c. and visceral adipose tissue and in muscle, but only muscle mRNA expression was decreased by fasting.

Adiponectin action from head to toe

“…Evidence for this assertion can be found in studies of various rodent models, where fasting, undernutrition and insulin deficiency lead to greater adiponectin sensitivity via increases in AdipoR expression [43,141,162]. In young growing pigs, fasting decreased the expression of T-cadherin but not AdipoR1/R2 in skeletal muscle [50]. On the other hand, adiponectin resistance resulted from decreased AdipoR expression under hyperglycemic and hyperinsulinemic conditions, in response to high-fat or high-sucrose feeding in rodent muscle and in genetically obese mice [141,158,161].…”

“…AdipoR1 and AdipoR2 transcripts and proteins are both detected in mice skeletal muscle with a predominant expression of the AdipoR1 gene over AdipoR2 [50,141,158,161]. Moreover, the expression of AdipoR1/R2 in the skeletal muscle appears to be inversely regulated by insulin in physiological and pathophysiological states such as fasting/refeeding, insulin deficiency and hyperinsulinemia models and therefore correlates with adiponectin sensitivity.…”

“…Moreover, in the rat carotid artery, the expression of T-cadherin is upregulated after injury caused by a balloon catheter [49] and, interestingly, T-cadherin and adiponectin are found in the same location in injured vessel walls [45]. Finally, the transcription of T-cadherin was found to be downregulated in skeletal muscles of 24-h-fasted pigs, suggesting a putative nutritional regulation of T-cadherin expression [50].…”

Gender-Specific Associations between Circulating T-Cadherin and High Molecular Weight-Adiponectin in Patients with Stable Coronary Artery Disease

“…SMC abundantly express T-cad and can also shed MPs [40]. T-cad is also expressed in adipose tissue [41] and was very recently identified (by ESI-LC-MS/MS proteomic profiling) as a novel component of the secretome of adipocytes isolated from murine visceral adipose tissue [42]. Moreover, levels of T-cad were much less abundant in the secretome from diabetes-susceptible mice [42], which is concordant with the previous finding of lower levels of T-cad in diabetic patients as compared to patients without diabetes [19].…”

Porcine Adiponectin Receptor 1 Transgene Resists High-fat/Sucrose Diet-Induced Weight Gain, Hepatosteatosis and Insulin Resistance in Mice

“…This laboratory has been interested in porcine adipose tissue lipid metabolism and its regulation, including studies of the cloned pAdipor1 and pAdipor2 . Our previous study found that both ADIPOR1 and ADIPOR2 were highly homologous between pigs and mice, and the receptors responded to insulin via the phosphatidylinositol 3-kinase (PI3K) pathway [10, 18, 19]. We have expressed the pADIPOR1 in mice in order to ascertain its metabolic functions and to be able to compare its functions to mADIPOR1.…”