Polar bear stress hormone cortisol fluctuates with the North Atlantic Oscillation climate index

Polar bears are heavily dependent on sea ice for hunting sufficient prey to meet their energetic needs. When the bears are left fasting, it may cause a rise in the levels of the stress hormone cortisol. Cortisol is the major corticosteroid hormone in most mammals, including polar bears. Production and regulation of this stress hormone are vital for the body as it is part of a myriad of processes, including in relation to metabolism, growth, development, reproduction, and immune function. In the present study, we examined the correlation between East Greenland polar bear hair cortisol concentration (HCC), a matrix that reflects longer-term hormone levels, and the fluctuations of the North Atlantic Oscillation (NAO) index, a large-scale climate phenomenon applied as a proxy for sea ice extent in the Greenland Sea along the coast of East Greenland. In doing so, a significant positive correlation (r = 0.88; p = 0.0004) was found between polar bear hair cortisol and the NAO, explaining 77 % of the variation in HCC observed between years over the period 1989-2009. This result indicates that interannual fluctuations in climate and ice cover have a substantial influence on longer-term cortisol levels in East Greenland polar bears. Further research into the implications and consequences inherent in this correlation are recommended, preferably across multiple polar bear populations

Metformin-induced glucagon-like peptide-1 secretion contributes to the actions of metformin in type 2 diabetes

Background: Metformin reduces plasma glucose and has been shown to increase glucagon-like peptide 1 (GLP-1) secretion. Whether this is a direct action of metformin on GLP-1 release, and whether some of the glucose-lowering effect of metformin occurs due to GLP-1 release, is unknown. The current study investigated metformin-induced GLP-1 secretion and its contribution to the overall glucose-lowering effect of metformin and underlying mechanisms in patients with type 2 diabetes. Methods: Twelve patients with type 2 diabetes were included in this placebo-controlled, double-blinded study. On 4 separate days, the patients received metformin (1,500 mg) or placebo suspended in a liquid meal, with subsequent i.v. infusion of the GLP-1 receptor antagonist exendin9-39 (Ex9-39) or saline. During 240 minutes, blood was sampled. The direct effect of metformin on GLP-1 secretion was tested ex vivo in human ileal and colonic tissue with and without dorsomorphin-induced inhibiting of the AMPK activity. Results: Metformin increased postprandial GLP-1 secretion compared with placebo (P = 0.014), and the postprandial glucose excursions were significantly smaller after metformin + saline compared with metformin + Ex9-39 (P = 0.004). Ex vivo metformin acutely increased GLP-1 secretion (colonic tissue, P < 0.01; ileal tissue, P < 0.05), but the effect was abolished by inhibition of AMPK activity. Conclusions: Metformin has a direct and AMPK-dependent effect on GLP-1-secreting L cells and increases postprandial GLP-1 secretion, which seems to contribute to metformin's glucose-lowering effect and mode of action.Emilie Bahne, Emily W.L. Sun, Richard L. Young, Morten Hansen, David P. Sonne, Jakob S. Hansen, Ulrich Rohde, Alice P. Liou, Margaret L. Jackson, Dayan de Fontgalland, Philippa Rabbitt, Paul Hollington, Luigi Sposato, Steven Due, David A. Wattchow, Jens F. Rehfeld, Jens J. Holst, Damien J. Keating, Tina Vilsbøll, and Filip K. Kno