No abstract is provided for this article.
No abstract is provided for this article.
Click to increase image sizeClick to decrease image sizeKey Words: abdominal obesitylipoproteinsdiabetesinsulin resistance
The objective of this paper is to review the current evidence in support of genetic factors underlying the clustering of components of the metabolic syndrome in obese individuals. It has become clear that individual features of the metabolic syndrome are partially determined by familial factors some of which are unique to a given component and others that are shared among several features. A few candidate genes, encoding proteins of glucose, insulin and lipid metabolism, lipolytic cascade, fatty acid intestinal absorption, glucocorticoid metabolism, haemostasis and blood pressure, have been associated with a clustering of metabolic abnormalities, although the functional significance of these associations remains to be established. Furthermore, genetic polymorphisms, such as those detected at several lipoprotein metabolism loci, can modulate the relationships between different components of the metabolic syndrome. An overfeeding study conducted on identical twins has demonstrated that genetic factors play an important role in the responsiveness to changing energy balance conditions. Leptin receptor, β2 adrenergic receptor and glucocorticoid receptor gene polymorphisms have been associated with an augmented clustering of metabolic abnormalities in response to overfeeding. Gene-gene interaction effects between markers of the α2A, β2 and β3 adrenergic receptor genes on components of the metabolic syndrome have been described. Genetic factors also seem to modify the responsiveness of metabolic syndrome features to endurance training. A growing understanding of the genetic architecture of the metabolic syndrome may help in the prevention of this condition. The reduction of excess body fat, the most common clinical feature among the cluster of metabolic abnormalities, should be the focus of the prevention and treatment of the metabolic syndrome.
No abstract is provided for this article.
PURPOSE Bouchard & Rankinen (2001) have described a dramatic range of response to a standard 20 week program of aerobic training. The purpose of the present study was to evaluate the potential contribution of experimental error to the magnitude of these inter-individual differences. METHODS The 2-week CV of individual VO2max readings was 5.1% (Skinner et al., 1999). Training response was estimated from paired measurements of VO2max taken before and after training in ˜ 52% of subjects (i.e., a CV of 3.6%), but if paired VO2max values differed by > 5%, the highest value was accepted (˜ 48% of subjects, CV 5.1%). RESULTS The weighted CV of VO2max for all subjects, as thus determined, was 4.3%. Assuming the 20-week CV matched the 2-week figure, the CV for test/retest data would be 6.1%, or (for an initial VO2max of 2159 ml/min) an SD of 132 ml/min. The previously reported inter-individual SD of training responses was 202 ml/min, age, gender and baseline values accounting for 11% of the total variance. The inter-individual SD after adjustment for these covariates was 191 ml/min. After allowing also for the likely measurement error of 132 ml/min (48% of residual variance), the SD due to inter-individual differences in training response decreased to 138 ml/min. CONCLUSION The likely explanation of the substantial residual inter-individual difference is a familial aggregation of training response. REFERENCES Bouchard C et al. J Appl Physiol 1999; 87: 1003–1008. Bouchard C, Rankinen T. Med Sci Sports Exerc 2001; 33: S446-S451. Skinner JS et al. Med Sci Sports Exerc 1999; 31: 1623–1628.
