Differential Effects of Thiazolidinediones on Adipocyte Growth and Recruitment in Zucker Fatty Rats

Background: Adipose tissue grows by two mechanisms: hyperplasia (cell number increase) and hypertrophy (cell size increase). Thiazolidinediones are insulin-sensitizing peroxisome proliferator-activated receptor gamma agonists that are known to affect the morphology of adipose tissue. Methodology: In this study, adipose cell-size probability distributions were measured in six Zucker fa/fa rats over a period of 24 days, from four weeks of age, using micro-biopsies to obtain subcutaneous (inguinal) fat tissue from the animals. Three of the rats were gavaged daily with rosiglitazone, a thiazolidinedione, and three served as controls. These longitudinal probability distributions were analyzed to obtain the rate of increase in cell-size diameter in rosiglitazone-treated animals, and the hyperplasia induced by treatment quantitatively. Conclusions: We found that treatment leads to hypertrophy that leads to an approximately linear rate of cell diameter increase (2 mm/day), and that the hyperplasia evident in treated animals occurs largely within the first eight days of treatment. The availability of additional lipid storage due to treatment may alleviate lipotoxicity and thereby promote insulin sensitivity. The hypothesis that a TZD regimen involving repeated treatments of limited duration may suffice for improvements in insulin sensitivity merits further investigation

Body mass index in young men and risk of inflammatory bowel disease through adult life: A population-based Danish cohort study

Abstract Body mass index (BMI) is associated with increased future risk of inflammatory bowel disease(IBD) particularly Crohn’s disease(CD), where associations with high and low BMI have been observed. Most studies are based on adult women. We aimed to explore the impact of BMI in men entering adult life on their long-term risk of developing IBD. A total of 377,957 men born during 1939–1959, with BMI measured at draft boards at mean age 19, were followed from 1977, or time of examination, to end of 2015. Risk of IBD was assessed using Cox regression. During 13 million person-years of follow-up, 1,523 developed CD and 3,323 UC. Using normal weight as reference, for CD the following HRs were observed: BMI < 18.5, 1.35; 95% CI, 1.12–1.62, BMI 25–29.9; 0.83; 95% CI, 0.68–1.02. and BMI > 30 1.20; 95% CI, 0.75–1.90). The increased risk of CD in underweight was maintained up until age 60 not explained by known effects of smoking. For UC, minor inverse associations were observed. Restricted cubic splines revealed a U-shape association between BMI and CD, but not UC. Low BMI of men entering adult life is associated with an increased incidence of CD and UC up to 40 years later

Growth in Height in Childhood and Risk of Coronary Heart Disease in Adult Men and Women

Peer reviewe

The Progressive Increase of Food Waste in America and Its Environmental Impact

Food waste contributes to excess consumption of freshwater and fossil fuels which, along with methane and CO2 emissions from decomposing food, impacts global climate change. Here, we calculate the energy content of nationwide food waste from the difference between the US food supply and the food consumed by the population. The latter was estimated using a validated mathematical model of metabolism relating body weight to the amount of food eaten. We found that US per capita food waste has progressively increased by ∼50% since 1974 reaching more than 1400 kcal per person per day or 150 trillion kcal per year. Food waste now accounts for more than one quarter of the total freshwater consumption and ∼300 million barrels of oil per year

Inactivation of the Rcan2 Gene in Mice Ameliorates the Age- and Diet-Induced Obesity by Causing a Reduction in Food Intake

Obesity is a serious international health problem that increases the risk of several diet-related chronic diseases. The genetic factors predisposing to obesity are little understood. Rcan2 was originally identified as a thyroid hormone-responsive gene. In the mouse, two splicing variants that harbor distinct tissue-specific expression patterns have been identified: Rcan2-3 is expressed predominately in the brain, whereas Rcan2-1 is expressed in the brain and other tissues such as the heart and skeletal muscle. Here, we show that Rcan2 plays an important role in the development of age- and diet-induced obesity. We found that although the loss of Rcan2 function in mice slowed growth in the first few weeks after birth, it also significantly ameliorated age- and diet-induced obesity in the mice by causing a reduction in food intake rather than increased energy expenditure. Rcan2 expression was most prominent in the ventromedial, dorsomedial and paraventricular hypothalamic nuclei governing energy balance. Fasting and refeeding experiment showed that only Rcan2-3 mRNA expression is up-regulated in the hypothalamus by fasting, and loss of Rcan2 significantly attenuates the hyperphagic response to starvation. Using double-mutant (Lepob/ob Rcan2−/−) mice, we were also able to demonstrate that Rcan2 and leptin regulate body weight through different pathways. Our findings indicate that there may be an Rcan2-dependent mechanism which regulates food intake and promotes weight gain through a leptin-independent pathway. This study provides novel information on the control of body weight in mice and should improve our understanding of the mechanisms of obesity in humans

Increasing Genetic Variance of Body Mass Index during the Swedish Obesity Epidemic

Peer reviewe

Increased Genetic Variance of BMI with a Higher Prevalence of Obesity

Peer reviewe

Familial Associations of Adiposity: Findings from a Cross-Sectional Study of 12,181 Parental-Offspring Trios from Belarus

It is suggested that maternal adiposity has a stronger association with offspring adiposity than does paternal adiposity. Furthermore, a recent small study reported gender assortment in parental-offspring adiposity associations. We aimed to examine these associations in one of the largest studies to date using data from a low-middle income country that has recently undergone a major political and economic transition.In a cross-sectional study of 12,181 parental-offspring trios from Belarus (mean age (SD) of mothers 31.7 (4.9), fathers 34.1 (5.1) and children 6.6 (0.3) at time of assessment), we found positive graded associations of mother's and father's BMI with offspring adiposity. There was no evidence that these associations differed between mothers and fathers. For example, the odds ratio of offspring overweight or obesity (based on BMI) comparing obese and overweight mothers to normal weight mothers was 2.03 (95%CI 1.77, 2.31) in fully adjusted models; the equivalent result for father's overweight/obesity was 1.81 (1.58, 2.07). Equivalent results for offspring being in the top 10% waist circumference were 1.91 (1.67, 2.18) comparing obese/overweight to normal weight mothers and 1.72 (1.53, 1.95) comparing obese/overweight to normal weight fathers. Similarly, results for offspring being in the top 10% of percent fat mass were 1.58 (1.36, 1.84) and 1.76 (1.49, 2.07), for mother's and father's obese/overweight exposures respectively. There was no strong or consistent evidence of gender assortment--i.e. associations of maternal adiposity exposures with offspring outcomes were similar in magnitude for their daughters compared to equivalent associations in their sons and paternal associations were also similar in sons and daughters.These findings suggest that genetic and/or shared familial environment explain family clustering of adiposity. Interventions aimed at changing overall family lifestyle are likely to be important for population level obesity prevention