Cancer incidence rates were slightly elevated in patients with acromegaly in our study, and this finding was supported by the meta-analysis of 23 studies, although it also suggested the presence of selection bias in some earlier studies.

ContextWomen show an accelerated loss of muscle mass around menopause, possibly related to the decline in estrogen. Furthermore, the anabolic response to resistance exercise seems to be hampered in postmenopausal women.ObjectiveWe aimed to test the hypothesis that transdermal estrogen therapy (ET) amplifies the skeletal muscle response to resistance training in early postmenopausal women.DesignA double-blinded randomized controlled study.SettingDepartment of Public Health, Aarhus University, Denmark.ParticipantsThirty-one healthy, untrained postmenopausal women no more than 5 years past menopause.Intervention(s)Supervised resistance training with placebo (PLC, n = 16) or transdermal ET (n = 15) for 12 weeks.Main Outcome Measure(s)The primary outcome parameter was a cross-sectional area of quadriceps femoris measured by magnetic resonance imaging, and secondary parameters were fat-free mass (dual-energy X-ray absorptiometry), muscle strength, and functional tests.ResultsThe increase in muscle cross-sectional area was significantly greater in the ET group (7.9%) compared with the PLC group (3.9%) (p < 0.05). Similarly, the increase in whole-body fat-free mass was greater in the ET group (5.5%) than in the PLC group (2.9%) (p < 0.05). Handgrip strength increased in ET (p < 0.05) but did not change in the PLC group. Muscle strength parameters, jumping height, and finger strength were all improved after the training period with no difference between groups.ConclusionThe use of transdermal ET enhanced the increase in muscle mass in response to 12 weeks of progressive resistance training in early postmenopausal women.

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Aims Hypoglycemia hinders optimal glycemic management in type 1 diabetes (T1D). Long diabetes duration and hypoglycemia impair hormonal counterregulatory responses to hypoglycemia. Our study was designed to test whether i) the metabolic responses and insulin sensitivity are impaired, and ii) affected by short-lived antecedent hypoglycemia in participants with T1D. Materials and Methods In a randomized, crossover, 2x2-factorial design, nine male participants with T1D and nine comparable control participants underwent 30 min hypoglycemia (p-glucose<2.9mmol/L) followed by a euglycemic clamp on two separate interventions: with and without 30 min hypoglycemia the day before the study day. Results During both interventions: insulin sensitivity was consistently lower, while counterregulatory hormones were reduced with 75% lower glucagon and 50% lower epinephrine during hypoglycemia in participants with T1D, who also displayed 40% lower lactate and 5-10-fold increased ketone bodies concentrations following hypoglycemia, whereas palmitate and glucose turnover, forearm glucose uptake and substrate oxidation did not differ between the groups. In participants with T1D, adipose tissue PTEN content, HSL phosphorylation and muscle GLUT4 content were decreased compared with controls. An antecedent hypoglycemic episodes lasting 30 minutes did not affect counter-regulation or insulin sensitivity. Conclusions Participants with T1D displayed insulin resistance, and impaired hormonal counter-regulation during hypoglycemia, whereas glucose and fatty acid fluxes were intact, and ketogenic responses amplified. We observed subtle alterations of intracellular signaling, and no effect of short-lived antecedent hypoglycemia on subsequent counter-regulation. This plausibly reflects the presence of insulin resistance, and implies that T1D is a condition with defective hormonal but preserved metabolic responsiveness to short-lived hypoglycemia.