(562.2) Effect of adrenalectomy and insulin resistance on non-shivering thermogenesis in the corpulent rat

Poster Board Number: E176

Orien Tulp (University of Science Arts amp; Technology, University of Science Arts amp; Technology, University of Science Arts amp; Technology), George Einstein (University of Science Arts amp; Technology, University of Science Arts amp; Technology, University of Science Arts amp; Technology), Aftab Awan (University of Health amp; Humanities Virgin Islands)

Glucocorticoid hormones have been reported to impede optimal insulin sensitivity and glucose uptake in peripheral tissues via interactions with GLUT transporters, leading to insulin resistance and impaired glucose uptake via GLUT transporters. The LA/Ntul//-cp rat expresses obesity in 25% of the offspring by 5 to 6 weeks of age but remains non diabetic throughout much if not all of its lifespan when normally reared. Groups of congenic lean and obese LA/Ntul//-cp rats were fed low glycemic Purina Chow diets from 6 to 9 weeks of age or overfed with a high energy cafeteria diet (Café) from 9 until 12 weeks of age. Subgroups of obese animals were adrenalectomized (ADX) at 6 weeks of age (WoA) and subjected to the same dietary regimen to determine if the Café overfeeding could enhance the normal thermic response to norepinephrine (NE) in the obese phenotype and to determine if ADX would result in a restoration of glycemic status and NE-induced thermogenesis in the obese phenotype. Measures of Oral Glucose Tolerance (OGT), Area under the glucose curve (AUC), and NE-stimulated VO2 were determined (NE, 200 µg, s.c.) at 6, 9 and 12 WoA in all treatment groups and Insulin:Glucose ratios (I:G) at 12 WoA. Obese animal demonstrated hyperphagia at all ages studied, and Obese ADX hyperphagia from 9 to 12 WoA. OGT and AUC indicated modest glucose intolerance in the obese phenotype, and which was restored following ADX at 6 and 9 WoA. NE resulted in a progressive increase in VO2 in lean rats at each age studied, but NE-stimulated VO2 was lower in the obese phenotype and decreased further after the Café feeding regimen. ADX was associated with a restoration of OGT, I:G and NE stimulated VO2 equivalent to that observed in lean animals at 12 weeks of age. These results are consistent with adrenocorticoid-mediated insulin resistance likely due to a receptor level defect in insulin sensitivity as a contributory factor in the impairment in OGT and NST in the obese phenotype of this strain.

Support or Funding Information

Supported by Institutional Resources of USAT Montserrat, UHHVI-BVI, and the Einstein Medical Institute, NPB, FL USA.

Supported by Institutional Resources of USAT Montserrat, UHHVI-BVI, and the Einstein Medical Institute, NPB, FL USA.