Our data confirm that both FFM and FM are significant contributors to BMR. When the effect of FM on BMR is removed, any association with leptin concentrations disappears, which suggests that previous links between circulating leptin concentrations and BMR occurred only because of inadequate control for the effects of FM.

The FTO gene has significant polymorphic variation associated with obesity, but its function is unknown. We screened a population of 150 whites (103F/47M) resident in NE Scotland, United Kingdom, for variants of the FTO gene and linked these to phenotypic variation in their energy expenditure (basal metabolic rate (BMR) and maximal oxygen consumption VO 2 max) and energy intake. There was no significant association between the FTO genotype and BMR or VO 2 max. The FTO genotype was significantly associated (P = 0.024) with variation in energy intake, with average daily intake being 9.0 MJ for the wild-type TT genotype and 10.2 and 9.5 MJ for the "at risk" AT and AA genotypes, respectively. Adjusting intake for BMR did not remove the significance (P = 0.043). FTO genotype probably affects obesity via effects on food intake rather than energy expenditure. Obesity (2008Obesity ( ) 16, 1961Obesity ( -1965Obesity ( . doi:10.1038Obesity ( /oby.2008 Obesity is a chronic condition associated with increases in the risk of type 2 diabetes, hypertension, cardiovascular disease, and various forms of cancer (1). Over the past 30 years, there has been a dramatic increase in the prevalence of obesity throughout the entire world (2). In the United States, for example, levels of obesity (BMI > 30 kg/m 2 ) in 1999-2002 were 32% of the adult population (3). Studies of mono-and di-zygotic twins have established that the variation in adult body fatness has a large genetic component (4-7).Studies of the regulation of food intake in rodent models of obesity have led to the identification of several cases where obesity is the consequence of single loss of function mutations in particularly important genes involved in regulation of body weight (8). However, these monogenic forms of obesity appear to be very rare (9). Over the past few years, several genes have been identified from wide-scale screening studies with common variants associated with differences in obesity. These studies include variants in the INSIG (10), GAD2 (11), ENPP1 (12), and FTO (13) genes. Attempts to replicate the effects of variants in the first three of these genes have met with variable success (14-16). However, the effect of polymorphic variation in the FTO gene (13), which was established in a genome-wide association study of a population of 1,924 type 2 diabetics combined with 2,938 controls, was replicated in 13 separate cohorts comprising almost 39,000 individuals. This verification lends strong support to the suggestion that this gene has common variants (the AA and AT genotypes) that predispose to obesity, relative to the wild (TT) genotype.The effect of genotype on BMI was detectable from 7 years old upward (1). Subsequent studies have confirmed the effect of the FTO variants on both obesity and diabetes (17,18).The FTO gene was originally cloned from a mutant mouse that had fused toes (Ft) (19) although the mutation in that instance included deletion of at least six separate genes, one of which was FTO. Expression studies indicate that FTO is widely expr...

1. With commercial selection for increased broiler performance there has been a correlated increase in the incidence of several metabolic disorders. A study was undertaken to investigate the balance between the unselected support tissues (including the heart, liver, spleen and the components of the gastrointestinal tract (GIT)) which drive growth in the selected demand tissues (eviscerated body mass) by assessing the genetic correlations between these traits. 2. Data were collected on 483 broiler birds taken from a commercial male broiler line with pedigree information. 3. Genetic parameters were estimated by restricted maximum likelihood with an individual animal model. Heritability estimates for the production traits ranged between h2 = 0.48 and 0.59 for leg and breast mass, respectively. The support tissues were generally associated with low to moderate heritabilities ranging between h2 = 0.19 for proventriculus to h2 = 0.38 for duodenum mass, although moderately high heritability estimates (h2 = 0.51 to 0.54) were associated with the spleen and gizzard. 4. The genetic correlations between production traits and support organs were generally low, however, heart mass was positively correlated with all carcase components of the lean tissue mass; the genetic correlations ranged between r(g) = 0.55 with breast mass to r(g) = 0.64 with eviscerated body mass. 5. In general, there were strong positive genetic correlations between the different components of the GIT. Organs that have been implicated in the development of metabolic disorders such as ascites (for example, the heart) could theoretically be used in commercial selection indices due to moderate heritabilities (heart: h2 = 0.30) and favourable correlations with commercially important traits.

These data are evidence of a gene x environment interaction for cognitive aging. They are relevant to the analysis of trials of n-3 PUFA supplements in cognitive aging and dementia prevention, and they support heterogeneity in cognitive aging and, possibly, in Alzheimer disease.