Maternal obesity at conception programs obesity in the offspring

Risk of obesity in adult life is subject to programming during gestation. To examine whether in utero exposure to maternal obesity increases the risk of obesity in offspring, we developed an overfeeding-based model of maternal obesity in rats utilizing intragastric feeding of diets via total enteral nutrition. Feeding liquid diets to adult female rats at 220 kcal/kg(3/4) per day (15% excess calories/day) compared with 187 kcal/kg(3/4) per day for 3 wk caused substantial increase in body weight gain, adiposity, serum insulin, leptin, and insulin resistance. Lean or obese female rats were mated with ad libitum AIN-93G-fed male rats. Exposure to obesity was ensured to be limited only to the maternal in utero environment by cross-fostering pups to lean dams having ad libitum access to AIN-93G diets throughout lactation. Numbers of pups, birth weight, and size were not affected by maternal obesity. Male offspring from each group were weaned at postnatal day (PND)21 to either AIN-93G diets or high-fat diets (45% fat calories). Body weights of offspring from obese dams did not differ from offspring of lean dams when fed AIN-93G diets through PND130. However, offspring from obese dams gained remarkably greater (P < 0.005) body weight and higher % body fat when fed a high-fat diet. Body composition was assessed by NMR, X-ray computerized tomography, and weights of adipose tissues. Adipose histomorphometry, insulin sensitivity, and food intake were also assessed in the offspring. Our data suggest that maternal obesity at conception leads to fetal programming of offspring, which could result in obesity in later life.     

肥胖孕妇肠道菌群与子代肥胖的相关性

妊娠期肥胖发生率在世界范围内呈上升趋势,成为影响人类健康的公共卫生问题。肥胖母亲肠道菌群失调导致婴儿早期定植菌群异常,而婴儿早期菌群定植情况与其日后生长发育密切相关,容易导致成年后出现肥胖、胰岛素抵抗、代谢综合征等疾病。因此针对肥胖孕妇肠道菌群分析,以及婴儿肠道菌群及生长发育的分析,对于孕妇孕期管理、健康宣教提高国民整体身体素质具有重要意义。     

Genetics of obesity

Considerable attention is currently being paid to the secular changes in food intake and physical activity that underlie the increase in the prevalence of obesity that is apparent in many societies. While this is laudable it would be unwise to view these environmental factors in isolation from the biological factors that normally control body weight and composition and the compelling evidence that inter-individual differences in susceptibility to obesity have strong genetic determinants. This is particularly important, as it is only in the past decade that we have begun to obtain substantive information regarding the molecular constituents of pathways controlling mammalian energy balance and therefore, for the first time, are in a position to achieve a better mechanistic understanding of this disease. Population-based association and linkage studies have highlighted a number of loci at which genetic variation is associated with obesity and related phenotypes and the identification and characterization of monogenic obesity syndromes has been particularly fruitful. While there is widespread acceptance that hereditary factors might predispose to human obesity, it is frequently assumed that such factors would influence metabolic rate or the selective partitioning of excess calories into fat. However, it is notable that, thus far, all monogenic defects causing human obesity actually disrupt hypothalamic pathways and have a profound effect on satiety and food intake. To conclude, the evidence we have to date suggests that the major impact of genes on human obesity is just as likely (or perhaps more likely) to directly impact on hunger, satiety and food intake rather than metabolic rate or nutrient partitioning. At the risk of oversimplification, it seems that from an aetiological/genetic standpoint, human obesity appears less a metabolic than a neuro-behavioural disease.     

Diet-induced obesity in zebrafish shares common pathophysiological pathways with mammalian obesity

Background  

Obesity is a multifactorial disorder influenced by genetic and environmental factors. Animal models of obesity are required to help us understand the signaling pathways underlying this condition. Zebrafish possess many structural and functional similarities with humans and have been used to model various human diseases, including a genetic model of obesity. The purpose of this study was to establish a zebrafish model of diet-induced obesity (DIO).     

Family functioning and obesity risk behaviors: implications for early obesity intervention

Family functioning is found to be associated with overweight and obesity in childhood, but its association with maternal obesity risk behaviors is not clear. This study aimed to investigate whether family functioning is associated with maternal obesity risk behaviors and to inform the development of early obesity interventions. A total of 408 first-time mothers at 24-34 weeks of pregnancy were included in the study. They participated in the Healthy Beginnings Trial (HBT) conducted in southwest Sydney, Australia in 2008. An analysis of cross-sectional baseline data was conducted using ordinal logistic regression modeling. Key measures were assessed using the McMaster Family Assessment Device, and self-reported obesity risk behaviors including excessive consumption of soft drinks, fast food, and excessive small screen time. The study found that 30% of the study population had a family functioning score ≥2, indicating unhealthy family functioning. About one-third (36%) of the mothers had more than one obesity risk behavior. Mothers with a family functioning score ≥2 were more likely to have more than one obesity risk behavior (47% vs. 32%, P < 0.05) than mothers with a lower score. The proportion of mothers with a family functioning score ≥2 increased from 22% to 29% to 39% as the number of maternal obesity risk behaviors increased from 0 to 1 to 2 or more, giving an adjusted proportional odds ratio (AOR) of 2.0 (95% confidence interval (CI) 1.3-3.0, P = 0.001). Family functioning is independently associated with the number of maternal obesity risk behaviors after allowing for the effects of maternal age and education. Overweight and obesity interventions should consider addressing family functioning.     

Financial hardship and obesity

There is a substantial correlation between household debt and health. Individuals with less healthy lifestyles are more likely to hold debt, yet there is little evidence as to whether this is merely a correlation or if financial hardship actually causes obesity. In this paper, we use data from the National Longitudinal Survey of Adolescent Health to test whether financial hardship affects body weight. We divide our sample into two groups: men and women, explore two different types of financial hardship: holding credit card debt and having trouble paying bills, and three outcomes: overweight, obese and body mass index (BMI). We use a variety of econometric techniques: Ordinary Least Squares, Propensity Score Matching, Sibling Fixed Effects, and Instrumental Variables to investigate the relationship that exists between financial hardship and body weight. In addition, we conduct several robustness checks. Although our OLS and PSM results indicate a correlation between financial hardship and body weight these results appear to be largely driven by unobservables. Our IV results suggest that there is no causal relationship between credit card debt and overweight or obesity for either men or women. However, we find suggestive evidence that having trouble paying bills may be a cause of obesity for women.