Cold Exposure Reverses the Diabetogenic Effects of High-Fat Feeding

Abstract

Long-term cafeteria feeding, cold exposure, and the combination of treatments increased energy intake in female Wistar rats by 25%, 113%, and 150%, respectively, in comparison with controls (P less than 0.01). Although cafeteria feeding at room temperature markedly increased the insulin response to an intravenous glucose tolerance test (IVGTT), glucose tolerance was deteriorated (P less than 0.01). In contrast, cold exposure significantly improved glucose tolerance in the presence of a reduced insulin response in Purina- and cafeteria-fed animals. Moreover, cold exposure also decreased body weight gain and increased brown adipose tissue mass, total cytochrome-oxidase activity, and cellularity by approximately 600-800%. The results suggest that cold exposure enhances insulin sensitivity of peripheral tissues, whereas hyperphagia on a high-fat, low-protein diet leads to insulin resistance. In addition, the results demonstrate that prolonged stimulation of energy expenditure by cold exposure not only reverses the diabetogenic effects of cafeteria feeding but also improves glucose tolerance. This phenomenon could result from a combination of two factors: (1) a cold-induced prevention of obesity; and (2) an enhanced disposal of circulating glucose into peripheral tissues, including brown adipose tissue.

HOXC10 suppresses browning of white adipose tissues

“…demonstrated that cold exposure improved the glucose clearance of rodents during a glucose tolerance test. 19 In agreement with the previous findings, control mice showed markedly improved glucose tolerance after cold exposure (Figure 2f). In mice expressing HOXC10, glucose disposal was less efficient compared with control mice (Figure 2f).…”

Paradoxical resistance to diet-induced obesity in UCP1-deficient mice

“…In this experiment with congenic mice (Table 4), there was no significant hyperglycemia detected in the wild-type mice, even though it is well established that B6 mice develop diabetes when fed this high-fat diet (20). Since this high-fat feeding experiment was conducted at reduced temperature, the increased energy expenditure to maintain body temperature probably reduced hyperglycemia, as previously described for rats fed a high-fat diet (21).…”

The apolipoprotein M/S1P axis controls triglyceride metabolism and brown fat activity

“…Mice Activated BAT protects against diet-induced obesity (Cawthorne et al, 1984;Peirce and Vidal-Puig, 2013;Vallerand et al, 1986). We, therefore, hypothesized that Apom À/À mice would (B and C) Mass of epiWAT (B) and BAT, including IsBAT and SubBAT (C) in wild-type (n = 6) mice and Apom À/À (n = 7) mice.…”

“…Hence, the present data should spark investigations to unravel a putative beneficial role of inhibiting the S1P 1 in, e.g., obesity and increased postprandial lipedema. Indeed, increased activity of BAT in humans has been associated with improved metabolic health from increased lipid metabolism, glucose uptake, and weight loss (Bartelt and Heeren, 2014;Cawthorne et al, 1984;Peirce and Vidal-Puig, 2013;Vallerand et al, 1986), and obese individuals also have reduced levels of BAT (van Marken Lichtenbelt et al, 2009). Inhibition of the apoM/S1P axis may provide a tool to address the extent to which stimulation of BAT is an effective means for improving metabolism in adult humans.…”