Meal-derived glucagon responses are related to lower hepatic phosphate concentrations in obesity and type 2 diabetes.

AIM: Type 2 diabetes (T2D) alters glucagon, glucagon-like peptide (GLP)-1, glucose-dependent insulinotropic polypeptide (GIP) and hepatic energy metabolism, yet the possible relationships remain unclear. METHODS: In this observational study, lean insulin-sensitive control subjects (BMI: 23.2±1.5kg/m2), age-matched insulin-resistant obese subjects (BMI: 34.3±1.7kg/m2) and similarly obese elderly T2D patients (BMI: 32.0±2.4kg/m2) underwent mixed-meal tolerance tests (MMTTs), and assessment of hepatic γATP, inorganic phosphate (Pi) and lipids using 31P/1H magnetic resonance spectroscopy. Meal-induced secretion of glucagon and incretins was calculated from incremental areas under the concentration-time curves (iAUCs). Peripheral and adipose tissue insulin sensitivity were assessed from time courses of circulating glucose, insulin and free fatty acids. RESULTS: MMTT-derived peripheral insulin sensitivity was lowest in T2D patients (P<0.001), while glucagon concentrations were comparable across all three groups. At 260min, GLP-1 was lower in T2D patients than in controls, whereas GIP was lowest in obese individuals. Fasting glucagon concentrations correlated positively with fasting (r=0.60) and postprandial hepatocellular lipid levels (160min: r=0.51, 240min: r=0.59), and negatively with adipose tissue insulin sensitivity (r=-0.73). Higher meal-induced glucagon release (iAUC0-260min) correlated with lower fasting (r=-0.62) and postprandial Pi levels (160min: r=-0.43, 240min: r=-0.42; all P<0.05). Higher meal-induced release of GIP (iAUC0-260min) correlated positively with fasting (r=0.54) and postprandial serum triglyceride concentrations (iAUC0-260min, r=0.54; all P<0.01). CONCLUSION: Correlations between fasting glucagon and hepatic lipids and between meal-induced glucagon and hepatic Pi suggest a role for glucagon in hepatic energy metabolism.

Effectiveness of current teaching methods in Cardiology: the SKILLS (medical Students Knowledge Integration of Lower Level clinical Skills) study.

INTRODUCTION: The aim of the study is to assess reported changes in medical students' capacity to attain five basic cardiological clinical skills, following a one-month intensive cardiology course provisioned in the core curriculum. MATERIALS AND METHODS: An anonymous questionnaire comprising self reported performance in the five skills, namely 1) arterial blood pressure measurement, 2) cardiac auscultation, 3) electrocardiogram (ECG) carry out, 4) ECG interpretation and 5) defibrillation, was distributed to 177 fifth year students of the Athens Medical School upon initiating the cardiology course (pre-training group) and to 59 students matched for sex, age, year of study and training centre, following completion of the course (post training group). Comparison of pre- and post- training performance was evaluated using the χ(2) test. RESULTS: No change was noted with regards to blood pressure measurement, cardiac auscultation or defibrillation. By contrast, a statistically significant improvement was reported for ECG execution (54.3 versus 81.4%; p<0.001) and interpretation (from 33.1 to 89.8%; p<0.001). CONCLUSIONS: Improvement in the execution and interpretation of ECGs seems to be among the strengths of the cardiology training program. Further studies including larger samples from multiple medical schools and objective assessment of skill execution might facilitate accurate training evaluation and define opportunities for improvement.

Adrenal incidentalomas and cardiometabolic morbidity: an emerging association with serious clinical implications.

Adrenal incidentalomas (AIs) represent adrenal masses that are incidentally discovered whilst investigating symptoms and signs unrelated to adrenal pathology. The onset and natural course of AIs are unknown, and the possible underlying cardiometabolic abnormalities have not been examined in depth. A growing body of clinical and experimental evidence supports the notion that both functioning and, paradoxically, nonfunctioning AIs are associated with a partially expressed or even full-blown metabolic syndrome (MS) phenotype, through yet unclear mechanisms. Subtle, subclinical or even profound adrenal hormone excess and an increased proinflammatory state might explain to some extent the development of MS disturbances. The emerging association between AIs and MS appears to be important in determining the optimal clinical management of these patients and raises speculation about the exact mechanisms of this interesting cause-effect relationship.