Adipose tissue is a primary site for lipid storage containing trace amounts of glycogen. However, re-feeding after a prolonged partial fast produces a marked transient spike in adipose glycogen, which dissipates in coordination with the initiation of lipid re-synthesis. To further study the potential interplay between glycogen and lipid metabolism in adipose tissue, the aP2-PTG transgenic mouse line was utilized, as it contains a 100-400-fold elevation of adipocyte glycogen levels that are mobilized upon fasting. In order to determine the fate of the released glucose-1-phosphate, a series of metabolic measurements were made. Basal and isoproterenol-stimulated lactate production in vitro was significantly increased in adipose tissue from transgenic animals. In parallel, basal and isoproterenol-induced release of non-esterified fatty acids (NEFAs) was significantly reduced in transgenic adipose tissue vs. control. Interestingly, glycerol release was unchanged between the genotypes, suggesting enhanced triglyceride re-synthesis was occurring in the transgenic tissue. Qualitatively similar results for NEFAs and glycerol levels between wild-type and transgenic animals were obtained in vivo during fasting. Additionally, the physiological up-regulation of PEPCK-C expression in adipose upon fasting was significantly blunted in transgenic mice. No changes in whole body metabolism were detected through indirect calorimetry. Yet, weight loss following a weight gain/loss protocol was completely blocked in the transgenic animals indicating a further impairment in triglyceride mobilization. Cumulatively, these results support the notion that the adipocyte possesses a set-point for glycogen which is altered in response to nutritional cues, enabling the coordination of adipose glycogen turn-over with lipid metabolism.
- Protein Phosphatase-1
- Copyright © 2009, American Journal of Physiology - Endocrinology and Metabolism