Nonshivering thermogenesis revisited: sympathetic and non-sympathetic contributions

Abstract

Factors of diet and environment contribute to complementary, additive mechanisms that influence the magnitude of diet induced thermogenesis generated in man and animals. Both short terms sympathetically mediated and longer acting thyroidal mediated pathways have been identified and appear to function in a metabolically coordinated fashion to facilitate biochemical and physiologic pathways of energy balance implicating multiple organs and peripheral tissues during periods of over- and under-nutrition. In a congenic lean rodent model known to express parameters of environmentally and diet induced mediated thermogenesis, thyroidal and sympathetic contributions each contributed to approximately 50% of the relative increase in VO2 in quietly resting animals after consuming a high energy palatable diet as determined in the presence vs. absence of α-methylparatyrosine, a sympathoplegic chemical agent. In contrast, in the obese phenotype of the corpulent and other rodent strains, both sympathetic and thyroidal contributions to adaptive thermogenic mechanisms are impaired in response to both nutritional and environmental challenge, contributing to a greater efficiency of energy metabolism and body fat accretion. Thus, the purpose of the present review is to approximate the qualitative distribution between the two primary factors linked to the physiologic process resulting in the expression of diet induced thermogenesis in a normally lean phenotype of rat, the LA/Ntul//-cp.

Glucocorticoid ablation restores glycemic and thermogenic parameters in obesity

“…While the specific biochemical mechanisms that contribute to the impaired capacity for not shivering thermogenesis and caloric expenditure in the obese phenotype remain unclear, the thermogenic defect is presumed to contribute to their enhanced caloric efficiency and contribute at least in part to their propensity for excess fat accretion and storage in adipose tissue depots. Dysregulation of glucocorticoid actions involving the insulin-dependent GLUT4 transporters and insulin insensitivity in addition to impaired thyroidal and sympathetic actions have been reported in the obese of several strains, and likely contribute a role in this animal model as well [9][10][11][12][20][21][22][23]. Regardless of the energy mechanisms involved, the LA/Ntul//-cp rat strain ranks among the longest surviving obese rat strains known due to the longevityprone Lister/Albany/NIH background, with the lean phenotype often surviving to 4 years or more and the obese littermates to 2.5 to 3 years under standard laboratory conditions [16][17][18][19].…”