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At least 523 records · Page 29Linked to original sources
PubMed1994

Child and parent psychological problems influence child weight control.

This study used path analytic methods to assess the influence of child psychopathology measured using the Child Behavior Checklist and parent psychiatric symptoms measured using the Cornell Medical Index on changes in child percent overweight in obese 8- to 11-year-old children over 2 years (6 months of treatment, 18 months of follow-up) provided family-based behavioral intervention. Path analysis for the 0-6 month change showed the influence of mother and father psychiatric symptoms and child age on child anxiety/depression scores that in turn influenced child percent overweight change during treatment, accounting for 41% of the shared variance. The path analysis for follow-up change showed mother and father psychiatric symptoms influenced child social problems at the first stage, and child social problems influenced child percent overweight change, accounting for 68.5% of the shared variance. These results provide the first demonstration that both parent and child problems may influence the short- and long-term success of obese children who participate in family-based behavioral treatment programs.

Adult↗
PubMed2001

Interleukin-15 mediates reciprocal regulation of adipose and muscle mass: a potential role in body weight control.

Interleukin (IL)-15 is a cytokine which is highly expressed in skeletal muscle. Cell culture studies have indicated that IL-15 may have an important role in muscle fiber growth and anabolism. However, data concerning the metabolic effects of this cytokine in vivo are lacking. In the present study, IL-15 was administered to adult rats for 7 days. While IL-15 did not cause changes in either muscle mass or muscle protein content, it induced significant changes in the fractional rates of both muscle protein synthesis and degradation, with no net changes in protein accumulation. Additionally, IL-15 administration resulted in a 33% decrease in white adipose tissue mass and a 20% decrease in circulating triacylglycerols; this was associated with a 47% lower hepatic lipogenic rate and a 36% lower plasma VLDL triacylglycerol content. The decrease in white fat induced by IL-15 was in adipose tissue. No changes were observed in the rate of lipolysis as a result of cytokine administration. These findings indicate that IL-15 has significant effects on both protein and lipid metabolism, and suggest that this cytokine may participate in reciprocal regulation of muscle and adipose tissue mass.

Adipose Tissue↗
PubMed2000

Role of substrate utilization and thermogenesis on body-weight control with particular reference to alcohol.

Alcohol (ethanol; EtOH) provides fuel energy to the body (29.7 kJ (7. 1 kcal)/g, 23.4 kJ (5.6 kcal)/ml), as do other macronutrients, but no associated essential nutrients. The thermogenic effect of EtOH (on average 15 % of its metabolizable value) is much greater than that of the main substrates utilized by the body, i.e. fat and carbohydrates (CHO), suggesting a lower net efficiency of energy utilization for EtOH than for fat and CHO. EtOH cannot be stored in the body and is toxic, so that there is an obligatory continuous oxidation of EtOH and it becomes the priority fuel to be metabolized. In contrast to CHO, its rate of oxidation does not depend on the dose ingested. As with CHO intake, it engenders a shift in postprandial substrate utilization (decrease in fat oxidation), but by a non-insulin-mediated mechanism. A limited amount of EtOH can be converted to fatty acids by hepatic de novo lipogenesis (as occurs with high levels of CHO feeding) from acetate production, which inhibits lipolysis in peripheral tissues. There is no evidence that EtOH consumed under normoenergetic conditions (i.e. isoenergetically replacing CHO or fat) leads to greater body fat storage than fat or CHO. However, there is still a lack of experimental studies on the influence of EtOH on the level of spontaneous physical activity in man. This effect may well depend on the dose of EtOH consumed as well as other intrinsic factors.

Alcohol Drinking↗
PubMed1996

Lifestyle modification: weight control, exercise, and smoking cessation.

Cigarette smoking, obesity, and sedentary lifestyle are known to increase risk of coronary and other vascular disease. Yet eliminating, or reducing, these risk factors through lifestyle modifications is a significant challenge to patients and their physicians. To help meet this challenge in patients with coronary and other vascular disease, physicians should use an approach similar to that followed in other treatment plans: First, help the patient understand the value of the therapy; second, discuss the way in which treatment will evolve and set appropriate goals; third, follow up by monitoring and encouraging the patient's progress and identifying any barriers or adverse effects. When applying this paradigm to exercise, physicians can motivate patients by making them aware of the benefit of even moderate levels of activity, outlining a specific exercise program and setting appropriate goals, and following up on their patients' progress. Studies show that physicians can have a major positive impact on smoking cessation merely by asking patients whether they smoke and advising smokers to quit. Physicians can further assist smokers by providing educational materials, referring patients to counseling groups when needed, and prescribing nicotine replacement therapy when appropriate. Again, follow-up is essential. Dietary intervention should be tailored to individual patients, their food preferences and ethnic backgrounds. Individuals should be encouraged to try a wide variety of nonfat and low-fat foods and incorporate those they find acceptable into their diet in place of higher-fat alternatives. Educational materials are helpful in motivating patients to modify their eating habits and in providing additional ideas for food substitutions.

Body Weight↗
PubMed1998

Substrate use during and following moderate- and low-intensity exercise: implications for weight control.

Substrate utilization during and after low- and moderate-intensity exercise of similar caloric expenditure was compared. Ten active males [age: 26.9 (4.8) years; height: 181.1 (4.8) cm; Mass: 75.7 (8.8) kg; maximum O2 consumption (VO2max): 51.2 (4.8) ml x kg(-1) x min(-1)] cycled at 33% and 66% VO2max on separate days for 90 and 45 min, respectively. After exercise, subjects rested in a recumbent position for 6 h. Two h post-exercise, subjects ate a standard meal of 66% carbohydrate (CHO), 11% protein, and 23% fat. Near-continuous indirect calorimetry and measurement of urinary nitrogen excretion were used to determine substrate utilization. Total caloric expenditure was similar for the two trials; however, significantly (P < 0.05) more fat [42.4 (3.6) g versus 24.0 (12.2) g] and less CHO [142.5 (28.5) g versus 188.8 (45.2) g] was utilized as a substrate during the low-intensity compared to the moderate-intensity trial. Protein utilization was similar for the two trials. The difference in substrate use can be attributed to the exercise period because over twice as much fat was utilized during low-intensity [30.0 (11.0) g] compared to moderate-intensity exercise [13.6 (6.6) g]. Significantly more (P < 0.05) CHO was utilized during the moderate-intensity [106.0 (27.8) g] compared to the low-intensity exercise [68.7 (20.0) g]. Substrate use during the recovery period was not significantly different. We conclude that low-intensity, long-duration exercise results in a greater total fat oxidation than does moderate intensity exercise of similar caloric expenditure. Dietary-induced thermogenesis was not different for the two trials.

Adult↗