Diet or exercise: The role of diet and/or exercise on changes of pro-inflammatory markers during a weight loss program in adult women with overweight.

BACKGROUND AND AIMS: Obesity is associated with increased inflammation leading to a higher risk for non-communicable diseases. There was a controversy about whether exercise has a better influence on reducing inflammation during a lifestyle modification program among individuals with obesity. The objective of this study was to evaluate whether exercise could provide a benefit in reducing inflammatory markers in the context of a weight loss program. METHODS: This is an experimental study with control. Subjects were pre-menopausal adult women with overweight and assigned for low-calorie diet only (LCD) or low-calorie diet and exercise (LCDex) without randomization. We compared the effect of LCDex (n = 36) and LCD (n = 36) on inflammation markers (leptin and interleukin 6/IL6) for 8 weeks. RESULTS: We showed that after the weight loss program, there was a significant increase in IL6 (p = 0.009) but no changes in leptin (p = 0.760) concentration in both groups. There were no difference in changes of IL6 between LCDex and LCD (p = 0.483). CONCLUSIONS: A weight loss program was associated with increased inflammation. Among premenopausal women with overweight, a combination of LCD with exercise does not provide a greater benefit in reducing inflammation than those with LCD alone. TRIAL REGISTRATION: KE/0700/06/2018.

The safety and efficacy of supervised exercise on pregnant women with overweight/obesity: A systematic review and meta-analysis of randomized controlled trials.

Behavioural modification through physical activity and dietary counselling has been shown to have beneficial effects on pregnant women with overweight/obesity. Whether exercise alone with supervision (ie, supervised exercise) may also benefit for pregnant women with overweight/obesity is still unknown. This systematic review and meta-analysis aimed to determine the safety and efficacy of supervised exercise on pregnant women with overweight/obesity. PubMed, Cochrane library, Embase (Ovid), CINAHL (EBSCO), and Web of Science were used to search publications using a combination of main keywords "obesity", "exercise", "pregnant women", and "randomised controlled trial". From a total of 740 publications, 11 randomized controlled trials were included. All studies reported no adverse effects of supervised exercise on pregnant women with overweight/obesity. Of interest, this meta-analysis showed gestational weight gain (GWG) was lower in the supervised exercise group as compared to control (Mean difference 0.88 kg, 95%CI -1.73 to -0.03, P = .04). There was a significant effect of supervised exercise on post-prandial blood glucose (MD: -0.24, 95%CI -0.47 to -0.01, P = .04) and insulin resistance (HOMA-IR) (MD: -0.18, 95%CI -0.30 to -0.05, P = .005). There were no differences in risk of gestational diabetes mellitus, pre-eclampsia/gestational hypertension, and newborn outcomes (eg, infants birth weight, preterm birth incident, and gestational age) (all P > .05). This meta-analysis might suggest beneficial effects of supervised exercise on pregnant women with overweight/obesity to prevent excessive GWG, attenuates insulin resistance, and the post-prandial blood glucose level.

The interaction between energy intake, physical activity and UCP2 -866G/A gene variation on weight gain and changes in adiposity: an Indonesian Nutrigenetic Cohort (INDOGENIC).

The present study aimed to investigate an interaction between energy intake, physical activity and UCP2 gene variation on weight gain and adiposity changes in Indonesian adults. This is a prospective cohort study conducted in 323 healthy adults living in the city of Yogyakarta, Indonesia. Energy intake, physical activity, body weight, BMI, percentage body fat and waist:hip ratio (WHR) were measured at baseline and after 2 years while UCP2 -866G/A gene variation was determined at baseline. We reported that after 2 years subjects had a significant increment in body weight, BMI, body fat and reduction in WHR (all P < 0·05). In all subjects, total energy intake was significantly correlated with changes in body weight (ß = 0·128, P = 0·023) and body fat (ß = 0·123, P = 0·030). Among subjects with the GG genotype, changes in energy intake were positively correlated with changes in body weight (ß = 0·232, P = 0·016) and body fat (ß = 0·201, P = 0·034). These correlations were insignificant among those with AA + GA genotypes (all P > 0·05). In summary, we show that UCP2 gene variation might influence the adiposity response towards changes in energy intake. Subjects with the GG genotype of UCP2 -866G/A gene were more responsive to energy intake, thus more prone to weight gain due to overeating.

The Interaction between Coffee: Caffeine Consumption, UCP2 Gene Variation, and Adiposity in Adults-A Cross-Sectional Study.

BACKGROUND: Coffee is suggested as an alternative option for weight loss but the relationship between coffee consumption and adiposity in population-based studies is still controversial. Therefore, this study was aimed at evaluating the relationship between coffee intake and adiposity in adults and to test whether uncoupling protein 2 (UCP2) gene variation was able to affect this relationship. METHODS: This was a cross-sectional study conducted in male and female adults living in the urban area of Yogyakarta, Indonesia. Adiposity was determined based on body weight, body mass index (BMI), percent body fat, and waist and hip circumference. Data on coffee consumption and other dietary components were collected using a semiquantitative food frequency questionnaire along with other caffeine-containing beverages such as tea, chocolate, and other beverages. The -866 G/A UCP2 gene variation was analyzed using polymerase chain reaction-restriction fragment length polymorphism. The correlation between coffee intake and adiposity was tested using linear regression test with adjustment for sex, age, energy intake, table sugar intake, and total caffeine intake. RESULTS: In all subjects, coffee intake was inversely correlated with body weight (ß = -0.122, p=0.028), BMI (ß = -0.157, p=0.005), and body fat (ß = -0.135, p=0.009). In subjects with AA + GA genotypes, coffee intake was inversely correlated with body weight (ß = -0.155, p=0.027), BMI (ß = -0.179, p=0.010), and body fat (ß = -0.148, p=0.021). By contrast, in subjects with GG genotype, coffee intake was not correlated with body weight (ß = -0.017, p=0.822), BMI (ß = -0.068, p=0.377), and body fat (ß = -0.047, p=0.504). CONCLUSION: We showed that coffee intake was negatively correlated with adiposity, and this was independent of total caffeine intake. Additionally, we showed that the -866 G/A UCP2 gene variation influences the relationship between coffee intake and adiposity.

Dietary Inflammatory Index Score and Its Association with Body Weight, Blood Pressure, Lipid Profile, and Leptin in Indonesian Adults.

It was previously reported that dietary intake is an important trigger for systemic inflammation and one of the lifestyle factors for the development of cardiovascular diseases. The aim of this study was to evaluate the association between Dietary Inflammatory Index (DII) score and body weight, blood pressure, lipid profile and leptin in an Indonesian population. This was a cross-sectional study conducted in 503 Indonesian adults. The DII score was calculated based on data of 30 nutrients and food components. Anthropometric profile, blood pressure, lipid profile, and leptin were measured. The association of these variables with the DII score was analyzed. The DII score was not associated with body weight, body mass index (BMI), body fat, waist circumference, hip circumference, systolic and diastolic blood pressure, triglycerides, and high-density lipoprotein (HDL) (both unadjusted and after adjustment for covariates). However, plasma leptin concentration was significantly associated with the DII score (B = 0.096, p = 0.020). Plasma leptin also increased significantly across tertiles of the DII score (ANCOVA, p = 0.031). This positive association between the DII score and plasma leptin concentration suggests a role for the inflammatory properties of the diet in regulating adipose tissue inflammation.

Obesity as the Sequel of Childhood Stunting: Ghrelin and GHSR Gene Polymorphism Explained.

Stunting or short stature in children is a significant nutritional problem in developing and underdeveloped countries. Stunting during childhood might affect brain development and impair development cognitive function. Additionally, this condition associated with the increased risk for obesity during adulthood. Several studies have shown that the increment risk of obesity and overweight in children with a short stature was due to their metabolic efficiency. Children with stunting have lower resting energy expenditure compared to non stunting children. Additionally, stunted children has higher respiratory quotient and carbohydrate oxidation but lower fat oxidation compared to non-stunting children. These results might explain why stunted children easily become obese, which is due to lower fat oxidation and leading to tendency to store fat.This review discussed the current status on studies in the nutrigenetic aspects of the relationship between stunting in the childhood and obesity in adulthood. I hypothesized that stunted children are more likely to become obese in their later life because they have lower metabolic rate and higher tendency of fat storage. There are several candidate genes and pathway involved in obesity and I suspected that ghrelin and its receptor growth hormone secretague receptor (GHSR) were responsible.

Dietary Intake after Weight Loss and the Risk of Weight Regain: Macronutrient Composition and Inflammatory Properties of the Diet.

Weight regain after successful weight loss is a big problem in obesity management. This study aimed to investigate whether weight regain after a weight loss period is correlated with the macronutrient composition and/or the inflammatory index of the diet during that period. Sixty one overweight and obese adults participated in this experimental study. Subjects lost approximately 10% of their initial weight by means of very low-calorie diet for five weeks, or a low calorie diet for 12 weeks. After that, subjects in both groups followed a strict weight maintenance diet based on individual needs for four weeks, which was followed by a nine-month weight maintenance period without dietary counseling. Anthropometrics and dietary intake data were recorded before weight loss (baseline) and during the weight maintenance period. On average, participants regained approximately half of their lost weight. We found no evidence that macronutrient composition during the weight maintenance period was associated with weight regain. The dietary inflammatory index (r = 0.304, p = 0.032) was positively correlated with weight regain and remained significant after correction for physical activity (r = 0.287, p = 0.045). Our data suggest that the inflammatory properties of diet play a role in weight regain after weight loss in overweight and obese adults.