The metabolic syndrome is characterised by insulin resistance and is a risk factor for cardiovascular disease. High fructose diets are implicated in the development of metabolic syndrome, because they result in de novo lipogenesis which results in an increase in very low density lipoprotein triglyceride transport to skeletal muscle. This saturated fat is thought to then cause insulin insensitivity in skeletal muscle tissue. In normal healthy individuals, it is known that ingestion of carbohydrate results in a sustained muscular sympathetic nervous response, as well as increases in systemic noradrenaline levels. This effects is theorised to be an effort to cause compensatory vasoconstriction in the periphery to maintain blood pressure in response to splanchnic vasodilation, and is thought to stimulate an increase in metabolic rate after feeding. However, in individuals with insulin resistance, this sympathetic nervous system activation may be impaired.
The effects of oral glucose loads on activation of the sympathetic nervous system has been investigated in insulin-resistant and insulin-sensitive obese subjects1. Subjects were pair matched to ensure similarities in sex, age and blood pressure. Researchers gave each subject 75 grams of glucose and measured muscle sympathetic nerve activity, insulin concentrations and systemic noradrenaline levels at 30, 60, 90 and 120 min. The results showed that subjects with insulin resistance has significantly greater insulin area under the curve from 0 to 120 min. Noradrenaline levels and muscle sympathetic nerve activity increased in insulin sensitive individuals after the glucose load, but in those subjects with insulin resistance there was a blunted and delayed sympathetic response. Body mass index, abdominal fat and insulin area under the curve were all independent and inverse predictors of sympathetic nervous system response.
The traditional view that obesity and weight gain is caused by a positive energy balance has been challenged by data collected in the last 50 years. Studies that investigate the effects of exercise on obesity continue to show that in a large number of obese individuals, long-term weight loss is not possible by increasing energy expenditure. In addition, calorie restriction in itself fails to cause long-term weight loss in a large number of obesity cases. Evidence suggests that obesity results from too many of the wrong types of food, that in turn cause metabolic changes that interfere with the normal postprandial metabolism of food. Improvements in diets, without calorie restriction, appear to be beneficial in these cases, which may make up a large proportion of the total number of obese individuals. This study supports the contention that insulin resistant individuals have metabolic abnormalities.
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