1,721,332 research outputs found
Hypertension, insulin resistance, and the metabolic syndrome
No full textImpaired glucose homeostasis, hypertriglyceridemia, low high-density lipoprotein cholesterol, high blood pressure, and central obesity tend to cluster in patients to generate a syndrome, the metabolic syndrome. In the adult population, the metabolic syndrome prevalence ranges between 15% and 25%. Poor fibrinolysis and low-grade inflammation also are associated with the metabolic syndrome, and they contribute to make it a condition that predisposes to cardiovascular disease. Insulin resistance and attendant hyperinsulinemia are the characteristic features of the metabolic syndrome and probably are responsible for impairment in glucose homeostasis, dyslipidemia, and higher blood pressure through cause-and-effect relationships. While awaiting the results of clinical trials with cardiovascular endpoints, we should treat the metabolic syndrome with aggressive lifestyle intervention and consider drugs that improve the whole cardiovascular risk profile
Effects of metformin and thiazolidinediones on suppression of hepatic glucose production and stimulation of glucose uptake in type 2 diabetes: a systematic review
No full textAims/hypothesis: Insulin resistance, which manifests itself as endogenous glucose overproduction and reduced insulin-mediated glucose uptake, is a core defect in type 2 diabetes. Metformin and the peroxisome proliferator-activated receptor-gamma agonists, the thiazolidinediones (TZDs), both lower glucose, although their mechanism of action is still subject to debate. This review analyses the evidence relevant to these mechanisms in vivo. Materials and methods: A systematic search of MEDLINE identified a total of 42 clinical studies that investigated the effects of TZDs (n=23) and/or metformin (n=19) on endogenous glucose production (using tracer glucose techniques) and peripheral glucose disposal (using the euglycaemic-hyperinsulinaemic clamp) in patients with type 2 diabetes (n=549). The original variables assessed were converted into standardised units and their mean group values were listed separately for open and placebo-controlled studies. Statistical analysis was scarried out, treating mean group values as individual values and comparing results (both as absolute values and percentage changes from baseline) across study categories (open vs placebo-controlled, TZDs vs metformin). Results: Both TZDs and metformin enhance insulin suppression of endogenous glucose production and fasting plasma glucose clearance. TZDs, but not metformin, also improve insulin-mediated glucose uptake at all insulin levels. Conclusions/interpretation: In patients with type 2 diabetes, metformin improves fasting hepatic insulin sensitivity and glucose clearance; TZDs improve fasting hepatic insulin sensitivity and glucose clearance, and potentiate glucose disposal under insulinised conditions
Is hyperglycemia a cardiovascular risk factor?
No full textPatients with diabetes show an increased vascular morbidity and mortality that reduces their life expectancy by ~5–15 years (depending on the age at diagnosis). There is convincing evidence from epidemiological and pathophysiological studies that hyperglycemia per se is largely responsible for the harmful effects of the disease. As recently shown by clinical trials, treatment of this condition may reduce cardiovascular events and mortality, and several therapies should be considered: initiating early and individualized treatment and avoiding hypoglycemia
A novel method for interpreting survival analysis data: description and test on three major clinical trials on cardiovascular prevention
No full textMajor results of randomized clinical trials on cardiovascular prevention are currently provided in terms of relative or absolute risk reductions, including also the number needed to treat (NNT), incorrectly implying that a treatment might prevent the occurrence of the outcome/s under investigation. Provided that these results are based on survival analysis, the primary measure of which is time-to-the outcome and not the outcome itself, we sought an alternative method to describe, analyse and interpret clinical trial results consistent with this assumption, so as to better define qualitative and quantitative heterogeneity of various therapeutic strategies in terms of their effects and costs
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