Tumor necrosis factor-alpha gene -308 G/A polymorphism modulates the relationship between dietary fat intake, serum lipids, and obesity risk in black South African women.

The prevalence of obesity and related disease risk is high in black South African (SA) women, possibly influenced by the dietary transition associated with urbanization. This study explored interactions between dietary fat intake and the tumor necrosis factor-alpha (TNFA) -308 G/A polymorphism on obesity, insulin resistance, and serum lipid concentrations in urbanized black SA women. Normal-weight (n = 105) and obese (n = 118) women underwent measurements of body composition, fat distribution, fasting serum lipids, glucose and insulin concentrations, and dietary intake. Participants were genotyped for the functional TNFA -308 G/A polymorphism. The genotype or allele frequency of the TNFA -308 G/A polymorphism did not differ between the BMI groups. However, when dietary fat intake was 30% of total energy intake [percentage energy (%E)], the odds of being obese with the TNFA GA+AA genotype was only 12% of that with GG, but increasing intake of dietary fat (%E) was associated with a significantly faster rate of increase in obesity risk in women with the TNFA GA+AA genotype compared with those with the GG genotype (P = 0.036). There were significant diet-gene interactions between alpha-linolenic acid (%E) and the total cholesterol:HDL-cholesterol ratio (P = 0.036), and PUFA (%E) and LDL cholesterol levels (P = 0.026), with participants with the A allele being more responsive to changes in relative fat intake. The TNFA -308 G/A polymorphism modified the relationship between dietary fat intake, obesity risk, and serum lipid concentrations in black SA women.

Conjugated linoleic acid isomers, t10c12 and c9t11, are differentially incorporated into adipose tissue and skeletal muscle in humans.

Conjugated linoleic acid (CLA) is a popular supplement believed to enhance immune function, body composition and insulin sensitivity, but results of scientific studies investigating its effects are conflicting. The isomer- and tissue-specific effects of CLA may explain these conflicting results. Therefore, this study quantified the incorporation of the c9t11 and t10c12 CLA isomers into adipose tissue and skeletal muscle in response to supplementation in healthy, regularly-exercising, non-obese persons. The CLA group (n = 14) ingested 3.9 g per day CLA (50:50 t9c11:c10t12) and the placebo group (n = 11) 3.9 g per day high-oleic-acid sunflower oil for 12 weeks. Following supplementation, the t10c12 isomer was incorporated into adipose tissue triacylglycerol (P < 0.001), and the c9t11 isomer tended to increase in skeletal muscle phospholipids (P = 0.056). Therefore, human adipose tissue and skeletal muscle are enriched with CLA in an isomer-specific manner.

Conjugated linoleic acid versus high-oleic acid sunflower oil: effects on energy metabolism, glucose tolerance, blood lipids, appetite and body composition in regularly exercising individuals.

The aim of this study was to measure the effects of 12 weeks of conjugated linoleic acid (CLA) supplementation on body composition, RER, RMR, blood lipid profiles, insulin sensitivity and appetite in exercising, normal-weight persons. In this double-blind, randomised, controlled trial, sixty-two non-obese subjects (twenty-five men, thirty-seven women) received either 3.9 g/d CLA or 3.9 g high-oleic acid sunflower oil for 12 weeks. Prior to and after 12 weeks of supplementation, oral glucose tolerance, blood lipid concentrations, body composition (dual-energy X-ray absorptiometry and computerised tomography scans), RMR, resting and exercising RER and appetite were measured. There were no significant effects of CLA on body composition or distribution, RMR, RER or appetite. During the oral glucose tolerance tests, mean plasma insulin concentrations (0, 30, 120 min) were significantly lower (P= 0.04) in women who supplemented with CLA (24.3 (SD 9.7) to 20.4 (SD 8.5) microU/ml) compared to high-oleic acid sunflower oil control (23.7 (SD 9.8) to 26.0 (SD 8.8) microU/ml). Serum NEFA levels in response to oral glucose were attenuated in both men and women in the CLA (P=0.001) compared to control group. However, serum total cholesterol and LDL-cholesterol concentrations decreased in both groups and HDL-cholesterol concentrations decreased in women over 12 weeks (P=0.001, P=0.02, P=0.02, respectively). In conclusion, mixed-isomer CLA supplementation had a favourable effect on serum insulin and NEFA response to oral glucose in non-obese, regularly exercising women, but there were no CLA-specific effects on body composition, energy expenditure or appetite.

The role of information processing between the brain and peripheral physiological systems in pacing and perception of effort.

This article examines how pacing strategies during exercise are controlled by information processing between the brain and peripheral physiological systems. It is suggested that, although several different pacing strategies can be used by athletes for events of different distance or duration, the underlying principle of how these different overall pacing strategies are controlled is similar. Perhaps the most important factor allowing the establishment of a pacing strategy is knowledge of the endpoint of a particular event. The brain centre controlling pace incorporates knowledge of the endpoint into an algorithm, together with memory of prior events of similar distance or duration, and knowledge of external (environmental) and internal (metabolic) conditions to set a particular optimal pacing strategy for a particular exercise bout. It is proposed that an internal clock, which appears to use scalar rather than absolute time scales, is used by the brain to generate knowledge of the duration or distance still to be covered, so that power output and metabolic rate can be altered appropriately throughout an event of a particular duration or distance. Although the initial pace is set at the beginning of an event in a feedforward manner, no event or internal physiological state will be identical to what has occurred previously. Therefore, continuous adjustments to the power output in the context of the overall pacing strategy occur throughout the exercise bout using feedback information from internal and external receptors. These continuous adjustments in power output require a specific length of time for afferent information to be assessed by the brain's pace control algorithm, and for efferent neural commands to be generated, and we suggest that it is this time lag that crates the fluctuations in power output that occur during an exercise bout. These non-monotonic changes in power output during exercise, associated with information processing between the brain and peripheral physiological systems, are crucial to maintain the overall pacing strategy chosen by the brain algorithm of each athlete at the start of the exercise bout.