Dietary and lifestyle factors contributing to insulin resistance

Abstract

The present review focuses on some aspects of diet and exercise behaviour as they affect insulin sensitivity in both diabetic and healthy subjects. Insulin resistance, a less than normal biological effect for a given insulin concentration, is present in a number of common conditions including non-insulin-dependent diabetes mellitus (NIDDM), essential hypertension, hypertriacylglycerolaemia and obesity. Evidence that insulin resistance may be important in the pathogenesis of these conditions, and the fact that they are frequently present in the same patient, has led to speculation that insulin resistance is a common aetiological factor (Reaven, 1988). There is also both epidemiological and experimental support for the view that raised circulating insulin concentrations, a consequence of impaired insulin sensitivity, are a risk factor for vascular disease (Pyorala, 1979; Ducimetiere et al. Stout, 1992). The ability of pharmacological agents used in the treatment of both MDDM and essential hypertension to alter insulin action is relevant to the choice of therapy in these diseases (Harper et al. 1996).Against this background of the potential importance of insulin resistance both to causation and treatment of common conditions, which carry a significant morbidity and mortality, effects of changes in diet and exercise upon insulin sensitivity are of considerable interest. In the present review only studies in human subjects are considered and the emphasis is on work where effects of insulin on glucose metabolism have been measured directly, usually involving the euglycaemic hyperinsulinaemic clamp technique. EXERCISE AND INSULIN SENSITIVITY IN MANOver 25 years ago Bjorntorp et al. (1970) demonstrated lower insulin concentrations in response to oral glucose in obese patients after a programme of exercise which improved physical fitness. The effects were independent of changes in body weight. Since blood glucose concentrations did not change, the lower circulating insulin concentrations were interpreted as indicating increased sensitivity to insulin. Bjorntorp et al. (1972) also showed in cross-sectional studies that fit subjects had lower insulin concentrations than less-fit individuals. Subsequent workers have measured whole-body insulin action directly using the euglycaemic hyperinsulinaemic clamp technique and confirmed that those exercising regularly are more insulin sensitive than sedentary subjects (Rosenthal et al. 1983).Improved insulin sensitivity follows a single bout of exercise and this effect wears off after 2-5 d (Schneider et al. 1984;Mikines et al. 1988Mikines et al. , 1989. It has been considered that acute effects probably account for most of the improvements in insulin sensitivity seen during physical training programmes. Thus, whilst training in association with weight loss improves insulin action (Bogardus et al. 1984), if weight is maintained by increased energy intake and the effect of the last bout of exercise is controlled, insulin sensitivity remains unaltered despite an improvement in cardio...

Early-life programming of susceptibility to dysregulation of glucose metabolism and the development of Type 2 diabetes mellitus

“…It is well established that key determinants of the onset of these metabolic diseases include genetic predisposition, together with adult lifestyle risk factors. Genetic predisposition has been assumed to play the major role in determining susceptibility to these diseases ; nevertheless, genetically susceptible individuals may not develop these diseases if adult lifestyle risk factors are avoided [1,2]. The ability to cope with the demands placed on metabolic systems by environmental factors varies between individuals, although how this is determined remains unclear.…”

Overweight and Metabolic and Hormonal Parameter Disruption Are Induced in Adult Male Mice by Manipulations During Lactation Period

“…Moreover, obesity is the main force in accelerating the increased incidence of type 2 diabetes mellitus, being the single most effective contributor to the pathogenesis of the disease: obesity and type 2 diabetes mellitus have epidemic diffusion and their incidence is rapidly increasing (4). One of the major determinants is a genetic predisposition; nevertheless, genetically susceptible individuals may not develop the disease, provided that they avoid certain risk factors (5). Among these risk factors, the importance of manipulations that induce modification of the metabolic programming such as growth deficit, determined by malnutrition during fetal and neonatal life, has been shown (6).…”