The one year exercise and lifestyle intervention program KLAKS: Effects on anthropometric parameters,cardiometabolic risk factors and glycemic control in childhood obesity

Objective

Regular physical exercise within structured lifestyle programs may improve weight status and minimize metabolic risk factors in childhood obesity. The aim of this study was to evaluate the effect of the one-year combined physical exercise/lifestyle program KLAKS on anthropometric and metabolic parameters and glycemic control in childhood obesity.

Materials and Methods

142 overweight/obese (BMI > 90th percentile) candidates (7–18 years) were enrolled, 115 participants completed the program. Anthropometrics and biochemical parameters were obtained at beginning and completion. An oral glucose tolerance test (OGTT) was performed in a subgroup of participants. Course of glucose and insulin levels within OGTT was correlated with several parameters and is reported here for those who completed the program.

Results

The mean standard deviation scores (SDS) decreased significantly for BMI, waist circumference, waist-to-height ratio (WHtR) and percentage body fat (all p ≤ 0.01). Improved metabolic risk markers included mean glucose levels within an OGTT at follow-up compared to baseline (p < 0.0001) and HbA1c (p = 0.05) as well as indications of improvement for gamma-glutamyl-transferase and free fatty acids.

Conclusions

The one-year combined exercise/lifestyle program KLAKS significantly improves markers of obesity and glycemic control. Impaired cardiometabolic risk markers, even subclinical, are also favorably influenced by program participation.     

The association of plant-based dietary patterns with visceral adiposity,lipid accumulation product,and triglyceride-glucose index in Iranian adults

BackgroundWe sought to investigate whether adherence to a more plant-based, and less animal-based, diet is associated with visceral adiposity, lipid accumulation product (LAP), and triglyceride-glucose index (TyG) in Iranian adults.MethodsThis cross-sectional study was conducted on 270 adults aged between 18–75 years old. We created three plant-based diets. including an overall plant-based diet index (PDI), hPDI, and uPDI based on tertiles regarding the intake of animal- or plant-based food items obtained from a semi quantitative food-frequency questionnaire.ResultsHigher hPDI was significantly associated with lower body mass index (BMI) (P-value = 0.01), lower waist circumference (P-value<0.001), and lower waist-hip ratio (P-value<0.001). A significant increase was found for high density lipoproteins (HDL) (P-trend <0.001) with a significant decrease for LAP (P-value = 0.03) in those with higher adherence to hPDI. Moreover, greater adherence to PDI was associated with a significant increase in diastolic blood pressure (DBP) (p-value = 0.01) and fat free mass (FFM) (p-value = 0.01). There were no significant associations between PDIs and TyG and VFA.ConclusionWe found that a higher hPDI score was significantly associated with better anthropometric measurements. A significant increase was found for HDL and a significant decrease was found for LAP on hPDI. However, a higher PDI score was significantly associated with higher DBP and higher FFM.     

电针配合耳穴贴压对肥胖伴多囊卵巢综合征患者血清胰岛素及睾酮的影响

目的:评价针刺配合耳穴贴压对肥胖女性伴多囊卵巢综合征的疗效,探讨其机制.方法:采用电针及耳穴贴压治疗肥胖女性伴有多囊卵巢综合征39例,体穴取天枢、丰隆、关元、四满等穴,耳穴取口、胃、脾等.3个疗程后,将患者疗效,治疗前后的体质量指数(BMI)、腰围(WC)以及血清中胰岛素(Ins)、睾酮(T)的变化进行对比.结果:39例患者中痊愈10例,有效25例,无效4例,总有效率达89.7%;患者的BMI、WC、Ins、T与治疗前对比均显著降低,差异均有统计学意义(均P＜0.01).结论:电针、耳穴贴压对肥胖女性伴有多囊卵巢综合征有较好的临床疗效,其治疗机制可能是通过对患者血清中胰岛素和睾酮的调节来实现的.     

Impact of birth weight and gender on early postnatal hypothalamic energy balance regulatory gene expression in the young lamb

Intra-uterine growth restriction (IUGR) is involved in developmental metabolic programming and here we test the hypothesis that IUGR affects the developing hypothalamic energy balance regulatory pathways in a sex-specific manner. This experiment investigated early postnatal hypothalamic gene expression for six primary leptin- and insulin-sensitive neuropeptides and receptors in male and female IUGR (n = 8 and 9, respectively) and normal (N) birth weight lambs (n = 8 per gender) gestated and suckled by overnourished mothers. IUGR lambs were smaller at birth, had increased fractional growth rates (FGR), lower final body weight (11 weeks) and similar body fat content compared with N lambs, while males had higher final body weight and insulinemia but lower body fat and leptinemia than females. In situ hybridization revealed greater gene expression in the hypothalamic arcuate nucleus at 11 weeks for anorexigenic genes in females and orexigenic genes in males, with no effect of IUGR. Leptinemia correlated with gene expression for neuropeptide Y (NPY, negatively) in both sexes and pro-opiomelanocortin (POMC, positively) in females but with leptin receptor (negatively) only in males. Current FGR for girth correlated negatively with gene expression for NPY in males and POMC in females. Neither IUGR nor gender affected suckling activity (proxy for appetite) assessed at 3 weeks, but final NPY gene expression correlated with suckling weight gain in males. This study has revealed no effect of IUGR on early postnatal hypothalamic energy balance gene expression but a major effect of gender associated with major sex differences in adiposity and leptinemia.     

Time-course of adiposity and fasting insulin from childhood to young adulthood in offspring of parents with coronary artery disease: the Bogalusa Heart Study

PURPOSE: Obesity and the attendant insulin resistance/hyperinsulinemia related to coronary artery disease (CAD) morbidity and mortality are well documented. However, information is lacking on the time-course relation of adiposity and fasting insulin from childhood to young adulthood in offspring of parents with CAD, a surrogate measure of future risk.

METHODS: Longitudinal analysis was performed on data collected from the Bogalusa Heart Study cohort with (n = 271) and without (n = 805) a parental history of CAD followed since childhood by repeated surveys from 1973 to 1991.

RESULTS: Lowess smoothing and multivariate analyses using Generalized Estimating Equations revealed that body mass index, triceps, and subscapular skinfolds were consistently higher from childhood to adulthood in offspring of parents with CAD history. Insulin levels during childhood and adolescence were lower in the offspring with affected parents. On the other hand, higher levels of fasting insulin from offspring were associated with positive parental history of CAD after age 20 and this association remained significant even after adjusting for body mass index. There was no significant interaction with race or sex in these relationships.

CONCLUSION: These results indicate that the offspring at high risk for CAD develop excess body fatness beginning in childhood and then later manifest hyperinsulinemia in young adulthood. These observations have important implications for prevention.     

Olanzapine affects locomotor activity and meal size in male rats

Olanzapine is an antipsychotic drug that frequently induces weight gain accompanied by increased fat deposition as a side effect. To investigate how olanzapine affects different aspects of energy balance, we used male rats to determine effects on meal patterns, food preference, locomotor activity and body temperature. In two short-term experiments olanzapine was administered via osmotic minipumps. In the first experiment, we offered rats standard lab chow only. In the second experiment, we offered rats free choice between chow, sucrose and saturated fat. In a third experiment, olanzapine was chronically administered via the drinking water to determine effects on body composition. In each experiment olanzapine decreased locomotor activity and altered meal patterns. Olanzapine caused an increase in average meal size accompanied by reduced meal frequency, without clearly affecting food preference. In the chronic experiment body composition was altered, favoring adipose tissue over lean muscle mass, despite reductions in overall body weight gain. The increase in average meal size implies that the primary effect of olanzapine on feeding is an impairment of the normal satiation process. Furthermore, energy balance is clearly affected by a reduction in locomotor activity. Thus, the effects of olanzapine on adiposity do not depend solely on the presence of hyperphagia.     

Dietary fat plays a major role in obesity: no

The percentage of dietary energy from fat has been suggested to be an important determinant of body fat, and this presumed effect has been invoked to justify the general promotion of low‐fat diets. Dietary fat and the prevalence of obesity are lower in poor countries than in affluent countries. However, these contrasts are seriously confounded by differences in physical activity and food availability; within areas of similar economic development, per capita intake of fat and the prevalence of obesity have not been positively correlated. Randomized trials are the preferable method for evaluating the effect of dietary fat on adiposity because they avoid problems of confounding that are difficult to control in other studies. In short‐term trials, a small reduction in body weight is typically seen in individuals randomized to diets with a lower percentage of calories from fat. In a meta‐analysis of these trials, it was estimated that a decrease in 10% of energy from fat would reduce weight by 16 g d^–1, which would correspond to a 9‐kg weight loss by 18 months. However, compensatory mechanisms appear to operate because in trials lasting one year or longer, fat consumption within the range of 18–40% of energy has consistently had little, if any, effect on body fatness. Moreover, within the United States (US), a substantial decline in the percentage of energy from fat during the last two decades has corresponded with a massive increase in obesity, and similar trends are occurring in other affluent countries. Diets high in fat do not account for the high prevalence of excess body fat in Western countries; reductions in the percentage of energy from fat will have no important benefits and could further exacerbate this problem. The emphasis on total fat reduction has been a serious distraction in efforts to control obesity and improve health in general.     

Early lead exposure and childhood adiposity in Mexico city

BackgroundPrenatal and early childhood lead exposures have been associated with reduced weight in infants and young children, while studies that have examined such associations in children during peripubescence are rare.ObjectivesWe investigated the associations of prenatal and early-life exposure to lead with indices of adiposity in peripubertal children living in Mexico City.MethodsMaternal bone lead (as a proxy for cumulative fetal exposure) was assessed at 1 month postpartum. Blood samples were obtained from children annually from 1 to 4 years. Multivariable linear regression models were used to examine the association between each lead biomarker and BMI z-score, waist circumference, sum of skinfolds and body fat percentage in 248 children aged 8–16 years.ResultsAfter adjusting for covariates, maternal patella lead was associated with lower child BMI z-score (β = ?0.02, 95% CI: 0.03, ?0.01, p = 0.004), waist circumference (β = ?0.12 cm, 95% CI: 0.22, ?0.03, p = 0.01), sum of skinfolds (β = ?0.29 mm, 95% CI: 0.50, ?0.08, p = 0.007) and body fat percentage (β = ?0.09%, 95% CI: 0.17, ?0.01, p = 0.03). No significant associations were detected from the postnatal exposure period.ConclusionsWe observed a significant and inverse association of prenatal lead exposure with body composition in Mexican children, suggesting the potential role of early lead exposure in the fetal programming of child growth. Further research on the biological mechanisms underlying these associations is needed.     

Influence of high-fat feeding, diet-induced obesity, and hyperamylinemia on the sensitivity to acute amylin

Obesity results in the increased secretion of various hormones controlling food intake and body weight, such as leptin, and insulin; increased circulating levels of pancreatic amylin have also been described in obese humans and rodents. Because leptin-resistance is present in diet-induced obese (DIO) rats, and because hyperleptinemia seems necessary for the full development of leptin resistance, we tested whether amylin sensitivity is inversely correlated with adiposity, such that DIO reduces the anorectic action of acute amylin. We also determined if hyperamylinemia leads to a change in amylin sensitivity. In the first experiment, rats were chronically exposed to a high fat (HF; 60% fat) diet or fed standard chow for control. The anorectic response to amylin was tested on several occasions over a 14 week observation period. HF feeding led to the expected increase in body adiposity; the response to an acute amylin injection (5 - 50 μg/kg s.c.) was unaltered for 10 weeks of HF feeding. Even after 12 weeks on a HF diet, which clearly caused obesity, acute administration of amylin (5 μg/kg, s.c.) was still able to suppress food intake, although the suppression was not statistically significant. Further experiments using additional doses of amylin will be necessary to demonstrate possible amylin resistance after HF feeding or in DIO rats. In the second experiment, we tested more specifically whether hyperamylinemia that may result from HF feeding and subsequent obesity, reduces the sensitivity of the amylin signaling system. To avoid confounding factors, we chronically infused lean chow fed rats with amylin (5 or 10 μg/kg/day s.c.) to elevate their plasma amylin concentration to levels observed in obese rats (30 - 40 pM). In the absence of obesity, hyperamylinemia did not lead to a reduced sensitivity to acute amylin (5 - 20 μg/kg s.c.) injections; acute amylin reduced eating similarly in all groups of rats. Overall, we concluded that direct diet effects by short term exposure to HF appear to be of little importance for amylin sensitivity; further, long-term maintenance on a HF diet and the resulting obesity only slightly attenuated the anorectic response to acute amylin. Because we observed no marked changes in amylin sensitivity in lean, chow fed rats with induced hyperamylinemia, amylin receptor downregulation in chronic hyperamylinemia does not seem to occur.     

Stephen C. Woods: a precocious scientist

To investigate the early scientific development of Steve Woods, I reviewed his research during the first decade after he received his doctoral degree in 1970. The main parts of his research program were conditioned insulin secretion and hypoglycemia, Pavlovian conditioning of insulin secretion before a scheduled access to food, and basal insulin as a negative-feedback signal from fat mass to the brain. These topics were pursued with experimental ingenuity; the resulting publications were interesting, clear, and rhetorically effective. Although the theoretical framework for his experiments with insulin was homeostatic, by the end of the decade he suggested that classic negative-feedback homeostasis needed to be revised to include learning acquired by lifestyle. Thus, Woods functioned as a mature scientist from the beginning of his research—he was very precocious. This precocity also characterized his teaching and mentoring as recalled by two of his students during that time, Joseph Vasselli and Paul Kulkosky. The most unusual and exemplary aspect of his precocity is that the outstanding performance of his first decade was maintained during the subsequent 30 years.