Recent Advances in the Management of Diabetes Mellitus

peer reviewedThe recent epidemic of type 2 diabetes and the recognition that achieving specific glycemic goals can reduce morbidity have made the effective treatment of hyperglycemia a priority. The new therapeutic agents and the development of algorithms for the adjustment of therapy might contribute to an improved management of the disease. Moreover, type 2 diabetes is frequently associated with other co-morbidities (obesity, hypertension, dyslipidaemia, prothrombotic state). The appropriate management of patients with type 2 diabetes requires a global approach targeting each risk factor in order to reduce cardiovascular morbidity and mortality. This challenge represents a major public health issue. In type 1 diabetes patients, intensive therapy such as in the Diabetes Control and Complications Trial (DCCT) has been shown to obtain long-term beneficial effects on the reduction of the risk of progressive retinopathy, neuropathy and nephropathy and of the risk of cardiovascular disease. This benefit reinforces the original DCCT message that intensive therapy should be implemented as early as possible in people with type 1 diabetes. The recent development of new insulin analogues and the technical improvements of portable insulin pumps might contribute to obtain such a better metabolic control.RÉSUMÉ : L’augmentation d’incidence, quasi épidémique, du diabète de type 2 et la démonstration que l’obtention de bons taux glycémiques permettait de réduire la morbidité ont fait du traitement de l’hyperglycémie une priorité. Le développement de nouvelles classes thérapeutiques et la mise au point d’algorithmes de traitement contribuent à améliorer cette prise en charge. De plus, le diabète de type 2 est souvent associé à d’autres comorbidités (obésité, hypertension artérielle, dyslipidémies, état pro-thrombotique). La prise en charge du patient diabétique de type 2 requiert une approche globale visant à corriger chaque facteur de risque, ce qui permet de réduire substantiellement la mortalité cardio-vasculaire. Cette stratégie doit être considérée comme un objectif majeur de santé publique. Chez le sujet diabétique de type 1, un traitement intensif, comme celui imposé dans l’étude DCCT, permet d’obtenir une réduction prolongée du risque de survenue et de progression de la rétinopathie, de la neuropathie, de la néphropathie ainsi que du risque de maladie cardio-vasculaire. Ce bénéfice persistant renforce le message initial de l’étude DCCT qui avait démontré que le traitement intensif du diabète de type 1 devait être instauré dès le début de la maladie. Le développement récent des analogues de l’insuline et les améliorations techniques des pompes à insuline portables pourraient contribuer à atteindre un meilleur contrôle métabolique

Effects of Regular Insulin or Insulin Lispro on Glucose Metabolism after an Oral Glucose Load in Patients with Type 2 Diabetes Mellitus

Seven obese Type 2 diabetic patients were studied for two 4-h periods after ingestion of a glucose load to determine the effects of preprandial subcutaneous injection of Insulin Lispro (5 min before the meal) or regular insulin (20 min before the meal) on glucose metabolism. Glucose production and utilisation were measured using a dual isotope method. After Lispro, the mean postprandial increase in plasma glucose was 29% lower and the increase in insulin concentration 25% higher than after regular insulin (p < 0.05). Suppression of endogenous glucose production was similar with both types of insulin. Thus, preprandial injection of Lispro reduced postprandial glucose increments in Type 2 diabetic patients as compared to regular insulin. This effect is best explained by the increased postprandial bioavailability of Lispro

Postprandial suppression of glucagon secretion depends on intact pulsatile insulin secretion - Further evidence for the intraislet insulin hypothesis

Type 2 diabetes is characterized by an similar to 60% loss of beta-cell mass, a marked defect in postprandial insulin secretion, and a failure to suppress postprandial glucagon concentrations. It is possible that postprandial. hyperglucagonemia in type 2 diabetes is due to impaired postprandial insulin secretion. To address this, we studied eight adult Goettingen minipigs before and after an -60% reduction in beta-cell mass induced by illoxan. Pigs were studied fasting and after ingestion of a mixed meal. Insulin and glucagon secretion were determined by deconvolution of blood hormone concentrations measured at 1-min intervals. The relationship between insulin and glucagon release was analyzed using cross-correlation and forward versus reverse cross-approximate entropy. We report that glucagon and insulin were secreted in similar to 4-min pulses. Prealloxan, postprandial insulin secretion drove an similar to 20% suppression of glucagon concentrations (P &lt; 0.01), through inhibition of glucagon pulse mass. The alloxan-induced similar to 60% deficit in beta-cell mass lead to an similar to 70% deficit in postprandia insulin secretion and loss of the postprandial insulin-driven suppression of glucagon secretion. We conclude that postprandial hyperglucagonemia in type 2 diabetes is likely due to loss of intraislet postprandial suppression of glucagon secretion by insulin

Selle turcique et fonction hypophysaire au cours des hypoyhyroïdies congénitales par ectopie ou hypogénésie thyroïdienne

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Postprandial suppression of glucagon secretion depends on intact pulsatile insulin secretion - Further evidence for the intraislet insulin hypothesis

Type 2 diabetes is characterized by an similar to 60% loss of beta-cell mass, a marked defect in postprandial insulin secretion, and a failure to suppress postprandial glucagon concentrations. It is possible that postprandial. hyperglucagonemia in type 2 diabetes is due to impaired postprandial insulin secretion. To address this, we studied eight adult Goettingen minipigs before and after an -60% reduction in beta-cell mass induced by illoxan. Pigs were studied fasting and after ingestion of a mixed meal. Insulin and glucagon secretion were determined by deconvolution of blood hormone concentrations measured at 1-min intervals. The relationship between insulin and glucagon release was analyzed using cross-correlation and forward versus reverse cross-approximate entropy. We report that glucagon and insulin were secreted in similar to 4-min pulses. Prealloxan, postprandial insulin secretion drove an similar to 20% suppression of glucagon concentrations (P &lt; 0.01), through inhibition of glucagon pulse mass. The alloxan-induced similar to 60% deficit in beta-cell mass lead to an similar to 70% deficit in postprandia insulin secretion and loss of the postprandial insulin-driven suppression of glucagon secretion. We conclude that postprandial hyperglucagonemia in type 2 diabetes is likely due to loss of intraislet postprandial suppression of glucagon secretion by insulin