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      Heart rate and the cardiovascular risk :

      ,
      Journal of Hypertension
      Ovid Technologies (Wolters Kluwer Health)

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          Banting lecture 1988. Role of insulin resistance in human disease.

          G M Reaven (1988)
          Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Incidence and precursors of hypertension in young adults: the Framingham Offspring Study.

            The occurrence of hypertension and its precursors is examined in the Framingham Offspring Study of 2,027 men and 2,267 women ages 20-49 years followed for 8 years. The age-specific prevalence of hypertension was similar at both the first (1971-1975) and the second (1979-1983) examination for both men and women. Prevalence rates were higher among men than among women, and there was a higher rate of hypertension treatment at the second exam, particularly among women, 75% of whom reported being treated for hypertension. The incidence of hypertension in participants free from hypertension at the first examination increased threefold from the second to the fifth age decades in men and eight-fold in women. Under age 40, men were twice as likely as women to develop hypertension, but after age 40, 8-year incidence rates were similar in men (14.2%) and women (12.9%). Adiposity, relative weight, heart rate, alcohol intake, hematocrit, blood sugar, serum protein, triglyceride, and phosphorous were all related to hypertension occurrence in one or both sexes, controlling for age. In multivariate analysis, adiposity (P less than 0.01), heart rate (P less than 0.01), and triglyceride (P less than 0.05) were all significant independent predictors of hypertension in men. In women, adiposity (P less than 0.001), heart rate (P less than 0.01), hematocrit (P less than 0.05), and alcohol consumption (P less than 0.05) were independent contributors. When controlling for blood pressure measured at the first examination, the best single predictor of hypertension incidence, the multivariate assessment changed very little. Adiposity stands out as a major controllable contributor to hypertension. Changes in body fat over 8 years were related to changes in both systolic and diastolic blood pressure. Markedly obese women in their fourth decade were seven times more likely to develop hypertension than were lean women of the same age. Weight control deserves a high priority in efforts to prevent hypertension in the general population.
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              Epinephrine-induced insulin resistance in man.

              Endogenous release of epinephrine after stress as well as exogenous epinephrine infusion are known to result in impaired glucose tolerance. Previous studies of man and animals have demonstrated that this effect of epinephrine results from inhibition of insulin secretion and augmentation of hepatic glucose production. However, the effect of epinephrine on tissue sensitivity to insulin, and the relative contributions of peripheral vs. hepatic resistance to impaired insulin action, have not been defined. Nine young normal-weight subjects were studied with the insulin clamp technique. Plasma insulin was raised by approximately 100 muU/ml while plasma glucose concentration was maintained at basal levels by a variable glucose infusion. Under these conditions of euglycemia, the amount of glucose metabolized equals the glucose infusion rate and is a measure of tissue sensitivity to insulin. Subjects received four studies: (a) insulin (42.6 mU/m(2).min), (b) insulin plus epinephrine (0.05 mug/kg.min), (c) insulin plus epinephrine plus propranolol (1.43 mug/kg.min), and (d) insulin plus propranolol. During insulin administration alone, glucose metabolism averaged 5.49+/-0.58 mg/kg.min. When epinephrine was infused with insulin, glucose metabolism fell by 41% to 3.26 mg/kg.min (P 100 muU/ml. When propranolol was administered with epinephrine, total glucose metabolism was restored to control values and hepatic glucose production suppressed normally. Propranolol alone had no effect on insulin-mediated glucose metabolism. These results indicate that epinephrine, acting primarily through a beta-adrenergic receptor, markedly impairs tissue sensitivity to an increase in plasma insulin levels, and that this effect results from both peripheral and hepatic resistance to the action of insulin.
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                Author and article information

                Journal
                Journal of Hypertension
                Journal of Hypertension
                Ovid Technologies (Wolters Kluwer Health)
                0263-6352
                1997
                January 1997
                : 15
                : 1
                : 3-17
                Article
                10.1097/00004872-199715010-00001
                9050965
                5e4c417b-5889-41a9-afec-e2a9d1a7a885
                © 1997
                History

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