[ Diabetes Type 1 ]

Diabetogenic action of GH and cortisol in insulin-dependent diabetes mellitus. Aspects of the mechanisms behind

Rates of splanchnic cortisol production equaled or exceeded those occurring in extrasplanchnic tissues (e.g. I tweeted her, it’s “because cortisol (stress hormone) increases when stressed”. A cross-sectional analysis was conducted among 757 participants (aged 65-90 years) of the population-based KORA (Cooperative Health Research in the Region of Augsburg)-Age study. Platelet markers were elevated in MD (F(6,60) = 11.14, p < .001) and T2DM (F(6,60) = 13.07, p < .001). To examine this, we quantified in vivo whole-body, splanchnic, and hepatic 11β-HSD1 activity in obese type 2 diabetic subjects. Basal and stimulated cortisol concentrations, DHEAS, and plasma renin activity (PRA) were measured. Upper arm segmental blood volume, estimated by an electrical impedance technique, was positively correlated with the cortisol to cortisone metabolite ratio in both the control subjects (r = 0.77; P < 0.05) and the IDDM patients in whom it was measured (r = 0.56; P < 0.05; n = 13), whereas the regression line was shifted leftward in IDDM (i.e. However, ACTH added to GH enhanced the diabetogenic effect of GH. The observed prevalence of CS in patients with T2DM varies widely between the different studies, ranging from 0-9.4%. While GH is essential in this respect the diabetogenic effect of cortisol is evident only in conjunction with GH.

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