Four types of human obesities are defined by topography of fat deposition. The focus of the paper is on the genetic determinants and the nongenetic correlates of the first type, which is commonly defined as excess weight-for-height or excess body fat without a particular concentration of fat in a given area of the body. The heritability of fat mass or percent body fat derived from underwater-weighing assessment of body density reaches '�-25% of the age- and gender-adjusted pheno- typic variance. The within-identical-twin-pair resemblance in the response to a standardized overfeeding protocol emphasizes the importance of the genotype in determining individual dif- ferences in body weight and body composition. In this regard, the proneness to store energy primarily as fat or as lean tissue is a major determinant of the response to a caloric sur- plus. Am J C/in Nutr 199l;53:l56lS-5S.
No abstract is provided for this article.
The evidence for common familial factors underlying total fat mass (estimated from underwater weighing) and abdominal visceral fat (assessed from CT scan) was examined in families participating in phase 2 of the Québec Family Study (QFS) using a bivariate familial correlation model. Previous QFS investigations suggest that both genetic (major and polygenic) and familial environmental factors influence each phenotype, accounting for between 55% to 71% of the phenotypic variance in fat mass, and between 55% to 72% for abdominal visceral fat The current study suggests that the bivariate familial effect ranges from 29% to 50%. This pattern suggests that there may be common familial determinants for abdominal visceral fat and total fat mass, as well as additional familial factors which are specific to each. The relatively high spouse cross‐trait correlations usually suggest that a large percent of the bivariate familial effect may be environmental in origin. However, if mating is not random, then the spouse resemblance may reflect either genetic or environmental causes, depending on the source [i.e., through similar genes or cohabitation (environmental) effects]. Finally, there are significant sex differences in the magnitude of the familial cross‐trait correlations involving parents, but not offspring, suggesting complex generation (i.e., age) and sex effects. For example, genes may turn on or off as a function of age and sex, and/or there may be an accumulation over time of effects due to the environment which may vary by sex. Whether the common familial factors are genetic (major and/or polygenic), environmental, or some combination of both, and whether the familial expression depends on sex and/or age warrants further investigation using more complex models.
In an attempt to associate genetic variation with endurance performance, red cell antigens ABO, MNSs, Rhesus, Duffy, Kell, P and red cell enzymes lactate dehydrogenase (EC: 1.1.1.27), malate dehydrogenase (EC: 1.1.1.37), phosphoglucomutasej (EC: 2.7.5.1) and phosphogluconate dehydrogenase (EC: 1.1.1.44) genetic systems were studied in 79 Caucasian athletes who participated in endurance sports during the 1976 Montreal Olympic Games. Gene frequencies were reported and phenotype frequencies were compared to appropriate reference populations. No significant differences were observed between the athletes and the nonathletic populations of reference. Comparisons of three genetic systems could be made with a sample of athletes from the 1968 Mexico Olympic Games. Phenotype frequencies were identical in the two samples of athletes. The search for genetic variants associated with endurance performance should continue for other genetic systems, particularly in skeletal muscle and other tissues related even more closely to this type of performance.
The 5-HT3 agonist 2-methyl-5-HT had previously been shown to enhance the electrically evoked release of [3H]5-HT from preloaded slices of the guinea pig brain. In the present study, 2-methyl-5-HT (1 microM) was also found to increase the K+ evoked release of [3H]5-HT from preloaded slices of the guinea pig hypothalamus and this effect was blocked by the selective 5-HT3 antagonist ondansetron. In the presence of tetrodotoxin, the enhancement of the K(+)-evoked release of [3H]5-HT by 2-methyl-5-HT in hypothalamus slices was blocked, thus suggesting that the 5-HT3 receptors mediating this effect are not located directly on 5-HT terminals. In agreement with this, 2-methyl-5-HT did not alter the K(+)-evoked release of [3H]5-HT in a synaptosomal preparation of the same brain structure, even at a concentration 10-fold greater than that used in the slices. Taken together, these data indicate that these facilitatory 5-HT3 receptors are not located on 5-HT terminals in the guinea pig hypothalamus and therefore are not autoreceptors.
