No abstract

We undertook this study to determine whether there are differences in the responses of different persons to long-term overfeeding and to assess the possibility that genotypes are involved in such differences. After a two-week base-line period, 12 pairs of young adult male monozygotic twins were overfed by 4.2 MJ (1000 kcal) per day, 6 days a week, for a total of 84 days during a 100-day period. The total excess amount each man consumed was 353 MJ (84,000 kcal). During overfeeding, individual changes in body composition and topography of fat deposition varied considerably. The mean weight gain was 8.1 kg, but the range was 4.3 to 13.3 kg. The similarity within each pair in the response to overfeeding was significant (P less than 0.05) with respect to body weight, percentage of fat, fat mass, and estimated subcutaneous fat, with about three times more variance among pairs than within pairs (r approximately 0.5). After adjustment for the gains in fat mass, the within-pair similarity was particularly evident with respect to the changes in regional fat distribution and amount of abdominal visceral fat (P less than 0.01), with about six times as much variance among pairs as within pairs (r approximately 0.7). We conclude that the most likely explanation for the intrapair similarity in the adaptation to long-term overfeeding and for the variations in weight gain and fat distribution among the pairs of twins is that genetic factors are involved. These may govern the tendency to store energy as either fat or lean tissue and the various determinants of the resting expenditure of energy.

Seven pairs of young adult male identical twins completed a negative energy balance protocol during which they exercised on cycle ergometers twice a day, 9 out of 10 days, over a period of 93 days while being kept on a constant daily energy and nutrient intake. The total energy deficit caused by exercise above tlie estimated energy cost of body weight maintenance readied 244 f 9.8 MJ (Mean f SEM).Baseline energy intake was estimated over a period of 17 days preceding the negative energy balance protocol. M e a n body weight loss was 5.0 kg (SEM = 0.6) (p < 0.001) and it was entirely accounted for by tlie loss of fat mass (p < 0.001). Fat-free mass was unchanged. Body energy losses reached 191 MJ (SEM = 24) (p < 0.001) wliicli represented about 78% of the estimated energy deficit. Subcutaneous fat loss was sliglitly more pronounced on the trunk than on the limbs as estimated from skinfolds, circumferences, and computed tomograpliy (CT). The reduction in CT-assessed abdominal visceral fat was quite striking, from 81 cm2 (SEM = 5) to 52 cm2 (SEM = 6) (p < 0.001). A t tlie same submaximal power output level, subjects oxidized more lipids than carbohydrates after tlie program as indicated by tlie changes in the respiratory exchange ratio (p 10.05). Intrapair resemblance was observed for tlie changes in body weight (p < 0.05), fat mass (P < 0.01), percent fat (p < 0.01), body energy content (p < 0.01), sum of 10 skinfolds (p < 0.01), abdominal visceral fat (p < 0.01), fasting plasma triglycerides (p < 0.05) and cliolesterol (p < 0.05), maximal oxygen uptake (p < 0.05), and respiratory exchange ratio during submaximal work (p < 0.01). We conclude that even though there were large individual differ- ences in response to the negative energy balance and exercise protocol, subjects with tlie same genotype were more alike in responses than sulljects with different genotypes particularly for, body fat, body energy, and abdominal visceral fat changes. High lipid oxidizers and low lipid oxidizers during submaximal exercise were also seen despite the fact that all subjects liad experienced tlie same exercise and nutritional conditions for about three montlis.

These results show that changes in the consumption of some specific food groups are associated with body-weight changes. Such specific eating patterns could help to improve obesity treatment and prevention.

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Background: Overweight and obesity have been associated with better survival in patients with chronic obstructive pulmonary disease (COPD). On the other hand, excess body weight is associated with abnormal metabolic and inflammatory profiles that define the metabolic syndrome and predispose to cardiovascular diseases. This study was undertaken to evaluate the impact of overweight and obesity on the prevalence of the metabolic syndrome and on the metabolic and inflammatory profiles in patients with COPD. Methods: Twenty-eight male patients with COPD were divided into an overweight/obese group [n ϭ 16, body mass index (BMI) ϭ 33.5 Ϯ 4.2 kg/m 2 ] and normal weight group (n ϭ 12, BMI ϭ 21.1 Ϯ 2.6 kg/m 2 ). Anthropometry, pulmonary function and body composition were assessed. The metabolic syndrome was diagnosed according to waist circumference, circulating levels of triglyceride and high-density lipoprotein cholesterol levels, fasting glycemia and blood pressure. C-reactive protein, tumor necrosis factor-␣ (TNF-␣), interleukin-6 (IL-6), leptin and adiponectin plasma levels were measured. Results: Airflow obstruction was less severe in overweight/obese compared with normal weight patients (forced expiratory volume 1 : 51 Ϯ 19% versus 31 Ϯ 12% predicted, respectively, P Ͻ 0.01). The metabolic syndrome was diagnosed in 50% of overweight/obese patients and in none of the normal weight patients. TNF-␣, IL-6 and leptin were significantly higher in overweight/obese patients whereas the adiponectin levels were reduced in the presence of excess weight. Conclusions:The metabolic syndrome was frequent in overweight/obese patients with COPD. Obesity in COPD was associated with a spectrum of metabolic and inflammatory abnormalities. (61%) of the metabolic syndrome in men with COPD participating to a pulmonary rehabilitation program. 13 In comparison, the reported prevalence of the metabolic syndrome in age-matched men without COPD is 44%. 14 Lastly, COPD may predispose to insulin resistance and type-II diabetes. 15 It therefore emerges that, although obesity may protect against mortality on the short term, the concomitant presence of COPD and obesity may define a clinical phenotype at a high risk for cardiovascular diseases. Before making recommendation about weight management in COPD, there is a need to better understand the implication of obesity in this specific patient population. We hypothesized that in the presence of overweight/ obesity, patients with COPD would exhibit a metabolic and inflammatory profile associated with a higher risk of cardiovascular diseases. This hypothesis was tested by evaluating the prevalence of the metabolic syndrome and characterizing the metabolic and inflammatory profile in overweight/obese patients with COPD in comparison to normal weight patients with COPD. Methods Subject characteristicsTwenty-eight male patients with COPD volunteered to participate in the study. These patients were recruited consecutively from a cohort of patients previously engaged in pulmonary rehabilitation in our inst...

The effect of overfeeding on energy expenditure was investigated in 23 young men subjected to a 353-MJ energy intake surplus over 100 d. The major part of this excess (222 MJ) was stored as body energy. The increase in energy cost of weight maintenance amounted to 52 MJ and was proportional to body weight gain. When it was added to the obligatory cost of fat and fat-free mass gains, the overall increase in energy expenditure amounted to a mean of 100 MJ. Four months after overfeeding, subjects had lost 82%, 74%, and 100% of the overfeeding gain in body weight, fat mass, and fat-free mass, respectively. We conclude that 1) in response to overfeeding, two-thirds of the excess energy intake is stored as body energy; 2) overfeeding induces an increase in energy cost of weight maintenance proportional to body weight gain, and 3) preoverfeeding energy balance tends to be restored when nonobese individuals return to their normal daily-life habits.

The genes involved in the serotonin system are major candidates in association studies on affective disorders and responses to antidepressants. We studied a functional polymorphism of the serotonin transporter (5-HTT) gene (a 44 bp insertion/deletion in the 5-HTT-linked polymorphic region (5-HTTLPR)) and lifetime history of antidepressant-induced mania (AIM) in a population of 305 patients with bipolar affective disorder. AIM was defined using a broad definition and a restrictive definition. No association was found between the 's' allele of the 5-HTTLPR and AIM for either definition. However, we found an association between the 5-HTTLPR and lifetime history of rapid cycling in a subsample of patients (for allele and genotype distributions: exact probability, p ¼ 0.0009 and w 2 ¼ 9.4; df ¼ 1; p ¼ 0.002, respectively). These results may help to explain the conflicting association results obtained with the 5-HTT gene polymorphism, in particular with AIM. Indeed, the precise phenotype associated with the 5-HTT gene is unclear. The association between the 's' allele and rapid cycling may provide further evidence for an association between the 5-HTTLPR 's' allele and a pattern of affective instability.