Exposure to fracking chemicals and wastewater spurs fat cell development: Researchers saw increases in the size and number of fat cells in laboratory models following exposure, even at diluted concentrations. -- ScienceDaily

Exposure to fracking chemicals and wastewater
promotes fat cell development, or adipogenesis, in living cells in a
laboratory, according to a new Duke University-led study.

Researchers observed increases in both the size and number of fat
cells after exposing living mouse cells in a dish to a mixture of 23
commonly used fracking chemicals. They also observed these effects after
exposing the cells to samples of wastewater from fracked oil and gas
wells and surface water believed to be contaminated with the wastewater.
The findings appear June 21 in Science of the Total Environment.

Minimizing exposure to common hormone-disrupting chemicals may reduce obesity rates -- ScienceDaily

Everyday products carry environmental chemicals that may be making us
fat by interfering with our hormones, according to research presented in
Barcelona at the European Society of Endocrinology annual meeting, ECE
2018. Following recommendations on how to avoid these chemicals could
help minimise exposure and potentially reduce the risk of obesity and
its complications.

Benefits of a healthy diet greater in people at high genetic risk for obesity: Genetic predisposition to obesity is no barrier to successful weight management -- ScienceDaily

The benefits of sticking to a healthy diet to prevent long term weight gain are greater in people at high genetic risk for obesity than in those with low genetic risk, finds a study in The BMJ today.

The researchers say their findings indicate that improving dietquality over time might lead to greater weight loss for people who are genetically susceptible to obesity. The study also indicates that the
genetic risk of weight gain is attenuated by improving diet quality.

Comment: In other words, certain susceptibility genes are no longer susceptibility genes when unhealthy eating is replaced by healthy eating.  

The paper is published in The British Medical Journal

Improving adherence to healthy dietary patterns, genetic risk, and long term weight gain: gene-diet interaction analysis in two prospective cohort studies

Gene-environment interaction study for BMI reveals interactions between genetic factors and physical activity, alcohol consumption and socioeconomic status

 "Previous genome-wide association studies (GWAS) have identified hundreds of genetic loci to be associated with body mass index (BMI) and risk of obesity. Genetic effects can differ between individuals depending on lifestyle or environmental factors due to gene-environment interactions. In this study, we examine gene-environment interactions in 362,496 unrelated participants with Caucasian ancestry from the UK Biobank resource. A total of 94 BMI-associated SNPs, selected from a previous GWAS on BMI, were used to construct weighted genetic scores for BMI (GSBMI). Linear regression modeling was used to estimate the effect of gene-environment interactions on BMI for 131 lifestyle factors related to: dietary habits, smoking and alcohol consumption, physical activity, socioeconomic status, mental health, sleeping patterns, as well as female-specific factors such as menopause and childbirth. In total, 15 lifestyle factors were observed to interact with GSBMI, of which alcohol intake frequency, usual walking pace, and Townsend deprivation index, a measure of socioeconomic status, were all highly significant (p = 1.45*10−29, p = 3.83*10−26, p = 4.66*10−11, respectively). Interestingly, the frequency of alcohol consumption, rather than the total weekly amount resulted in a significant interaction. The FTO locus was the strongest single locus interacting with any of the lifestyle factors. However, 13 significant interactions were also observed after omitting the FTO locus from the genetic score. Our analyses indicate that many lifestyle factors modify the genetic effects on BMI with some groups of individuals having more than double the effect of the genetic score. However, the underlying causal mechanisms of gene-environmental interactions are difficult to deduce from cross-sectional data alone and controlled experiments are required to fully characterise the causal factors."



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Nonnutritive sweeteners and cardiometabolic health: a systematic review and meta-analysis of randomized controlled trials and prospective cohort studies

 BACKGROUND Nonnutritive sweeteners, such as aspartame, sucralose and stevioside, are widely consumed, yet their long-term health impact is uncertain. We synthesized evidence from prospective studies to determine whether routine consumption of non-nutritive sweeteners was associated with long-term adverse cardiometabolic effects. 

METHODS We searched MEDLINE, Embase and Cochrane Library (inception to January 2016) for randomized controlled trials (RCTs) that evaluated interventions for nonnutritive sweeteners and prospective cohort studies that reported on consumption of non-nutritive sweeteners among adults and adolescents. The primary outcome was body mass index (BMI). Secondary outcomes included weight, obesity and other cardiometabolic end points.

 RESULTS From 11 774 citations, we included 7 trials (1003 participants; median follow-up 6 mo) and 30 cohort studies (405 907 participants; median follow-up 10 yr). In the included RCTs, nonnutritive sweeteners had no significant effect on BMI (mean difference −0.37 kg/m2; 95% confidence interval [CI] −1.10 to 0.36; I2 9%; 242 participants). In the included cohort studies, consumption of nonnutritive sweeteners was associated with a modest increase in BMI (mean correlation 0.05, 95% CI 0.03 to 0.06; I2 0%; 21 256 participants). Data from RCTs showed no consistent effects of nonnutritive sweeteners on other measures of body composition and reported no further secondary outcomes. In the cohort studies, consumption of nonnutritive sweeteners was associated with increases in weight and waist circumference, and higher incidence of obesity, hypertension, metabolic syndrome, type 2 diabetes and cardiovascular events. Publication bias was indicated for studies with diabetes as an outcome.

 INTERPRETATION Evidence from RCTs does not clearly support the intended benefits of nonnutritive sweeteners for weight management, and observational data suggest that routine intake of nonnutritive sweeteners may be associated with increased BMI and cardiometabolic risk. Further research is needed to fully characterize the long-term risks and benefits of nonnutritive sweeteners. Protocol registration: PROSPERO-CRD42015019749"



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Characterization of Adipogenic Activity of House Dust Extracts and Semi-Volatile Indoor Contaminants in 3T3-L1 Cells - Environmental Science & Technology (ACS Publications)

  "Obesity and metabolic disorders are of great societal concern and generate significant human health care costs. Recently, attention has focused on the potential for environmental contaminants to act as metabolic disruptors. This study sought to evaluate the adipogenic activity of indoor house dust extracts and a suite of semivolatile organic chemicals (SVOCs) that are often ubiquitously detected in indoor environments. 3T3-L1 cells were exposed to extracts of indoor dust or individual SVOCs and assessed for triglyceride accumulation and preadipocyte proliferation. Ten of 11 house dust extracts exhibited significant triglyceride accumulation and/or proliferation at environmentally relevant levels (<20 μg of dust/well), and significant adipogenic activity was also exhibited by 28 of the SVOCs. Notably, pyraclostrobin, dibutyl phthalate, tert-butyl-phenyl diphenyl phosphate, and the isopropylated triaryl phosphates (ITPs) exhibited near maximal or supra-maximal triglyceride accumulation relative to the rosiglitazone-induced maximum. The adipogenic activity in house dust occurred at concentrations below EPA estimated child exposure levels, and raises concerns for human health impacts, particularly in children. Our results delineate a novel potential health threat and identify putative causative SVOCs that are likely contributing to this activity."



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Erythritol is a pentose-phosphate pathway metabolite and associated with adiposity gain in young adults

 "The prevention of weight gain in adulthood is a public health challenge, particularly given the difficulty of losing weight. Data on freshmen were collected at the beginning and end of the academic year, and baseline blood samples were studied to find markers of incident weight gain. A metabolite, erythritol, was elevated at the beginning of the year in freshmen who went on to gain weight, fat, and abdominal fat compared with freshmen with stable weight. Erythritol is a sugar substitute low-calorie sweetener, and prior studies claimed no endogenous synthesis. We report a previously unrecognized metabolism of glucose to erythritol, and given the association between erythritol and weight gain, research is needed to understand whether and how this pathway contributes to weight gain risk."

Low-calorie sweeteners promote fat accumulation in human fat

 "Low-calorie, artificial sweeteners appear to play havoc with the body's metabolism, and large consumption of these sugar substitutes could promote fat accumulation, especially in people who are already obese, preliminary research suggests. The study results will be presented Monday at ENDO 2017, the Endocrine Society's 99th annual meeting in Orlando, Fla."



 Sen and his colleagues tested sucralose, a popular low-calorie sweetener, on stem cells—cells that could change into mature fat, muscle, cartilage or bone cells—taken from human fat tissue. They placed these cells in Petri dishes for 12 days in media that promotes fat production. At a 0.2-millimolar sucralose dose similar to the concentration found in the blood of people with high consumption of low-calorie sweeteners—equal to four cans of diet soda per day—the researchers said they observed increased expression of genes that are markers of fat production and inflammation. There also was increased accumulation of fat droplets in cells, particularly at a larger dose (1 millimolar), Sen reported.

Prenatal bisphenol A exposure weakens body's fullness cues

The new study found mice born to mothers exposed to bisphenol A were less responsive to the hormone leptin, which is sometimes called the satiety hormone. Leptin helps inhibit the appetite by reducing hunger pangs when the body does not need energy. The hormone sends signals to the hypothalamus region of the brain to suppress the appetite.
"Our findings show that bisphenol A can promote obesity in mice by altering the hypothalamic circuits in the brain that regulate feeding behavior and energy balance," said the study's senior author, Alfonso Abizaid, Ph.D., of the Department of Neuroscience at Carleton University in Ottawa, Canada. "Low level prenatal exposure to BPA delays a surge of leptin after birth that allows mice to develop the proper response to the hormone. BPA exposure permanently alters the neurobiology in the affected mice, making them prone to obesity as adults.



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The type, not just the amount, of sugar consumption matters in risk of health problems

Female rats were given a liquid solution of either glucose (a form of sugar found naturally in the body after carbohydrates are broken down) or fructose (sugar found in fruit and fruit juices) in addition to their normal diet of solid food. The rats received the sweetened solutions for eight weeks, roughly equivalent to a person eating large amounts of sugar for six years. The sugar-fed rats were compared with a control group that received plain drinking water in addition to their food supply.
Researchers found that although both sugar-fed groups consumed more calories than the control group, the total calorie intake of the glucose-fed rats was higher than the rats that were given fructose. Another surprising observation was that "despite this difference, only the fructose group exhibited a significant increase in final body weight," wrote the research team.
In addition to higher weight gain, the fructose group showed more markers of vascular disease and liver damage than the glucose group. These included high triglycerides, increased liver weight, decreased fat burning in the liver (a factor that can contribute to fatty liver) and impaired relaxation of the aorta, which can affect blood pressure."

A purified membrane protein from Akkermansia muciniphila or the pasteurized bacterium improves metabolism in obese and diabetic mice : Nature Medicine : Nature Research

 Obesity and type 2 diabetes are associated with low-grade inflammation and specific changes in gut microbiota composition1, 2, 3, 4, 5, 6, 7. We previously demonstrated that administration of Akkermansia muciniphila to mice prevents the development of obesity and associated complications8. However, the underlying mechanisms of this protective effect remain unclear. Moreover, the sensitivity of A. muciniphila to oxygen and the presence of animal-derived compounds in its growth medium currently limit the development of translational approaches for human medicine9. We have addressed these issues here by showing that A. muciniphila retains its efficacy when grown on a synthetic medium compatible with human administration. Unexpectedly, we discovered that pasteurization of A. muciniphila enhanced its capacity to reduce fat mass development, insulin resistance and dyslipidemia in mice. These improvements were notably associated with a modulation of the host urinary metabolomics profile and intestinal energy absorption. We demonstrated that Amuc_1100, a specific protein isolated from the outer membrane of A. muciniphila, interacts with Toll-like receptor 2, is stable at temperatures used for pasteurization, improves the gut barrier and partly recapitulates the beneficial effects of the bacterium. Finally, we showed that administration of live or pasteurized A. muciniphila grown on the synthetic medium is safe in humans. These findings provide support for the use of different preparations of A. muciniphila as therapeutic options to target human obesity and associated disorders.

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Aspartame may prevent, not promote, weight loss by blocking intestinal enzyme's activity: Study identifies possible mechanism behind sugar substitute's lack of effectiveness -- ScienceDaily

A team of Massachusetts General Hospital (MGH) investigators has found a possible mechanism explaining why use of the sugar substitute aspartame might not promote weight loss. In their report published online in Applied Physiology, Nutrition and Metabolism, the researchers show how the aspartame breakdown product phenylalanine interferes with the action of an enzyme previously shown to prevent metabolic syndrome -- a group of symptoms associated with type 2 diabetes and cardiovascular disease. They also showed that mice receiving aspartame in their drinking water gained more weight and developed other symptoms of metabolic syndrome than animals fed similar diets lacking aspartame.

Aspartame blocks a gut enzyme called intestinal alkaline phosphatase (IAP) that we previously showed can prevent obesity, diabetes and metabolic syndrome; so we think that aspartame might not work because, even as it is substituting for sugar, it blocks the beneficial aspects of IAP

Genetic risk for obesity grew stronger in 'obesogenic' environment

Lending support to the idea that high-calorie diets, sedentariness and other aspects of the contemporary American lifestyle may be driving the obesity epidemic, UC San Francisco researchers have found that people who carry greater genetic risk for obesity were more likely to have a higher body mass index if they were born later in the 20th century.

The study, published Tuesday, July 5 in JAMA, looked at 7,482 white and 1,306 black participants in the U.S. nationwide Health and Retirement Study who were born between 1900 and 1958. Researchers calculated a genetic risk score for each participant, based on whether they had any of 29 genetic variants that are associated with obesity, and looked to see how this score compared with their BMI.

The number of variants each person had did not increase in the population over time, while their effects on people did, pointing to environmental influences. 

Association Between Artificially Sweetened Beverage Consumption During Pregnancy and Infant Body Mass Index: JAMA Pediatrics

Importance
The consumption of artificial sweeteners has increased substantially in recent decades, including among pregnant women. Animal studies suggest that exposure to artificial sweeteners in utero may predispose offspring to develop obesity; however, to our knowledge, this has never been studied in humans.
 Objective  To determine whether maternal consumption of artificially sweetened beverages during pregnancy is associated with infant body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]).
Design, Setting, and Participants  This cohort study included 3033 mother-infant dyads from the Canadian Healthy Infant Longitudinal Development (CHILD) Study, a population-based birth cohort that recruited healthy pregnant women from 2009 to 2012. Women completed dietary assessments during pregnancy, and their infants’ BMI was measured at 1 year of age (n = 2686; 89% follow-up). Statistical analysis for this study used data collected after the first year of follow-up, which was completed in October 2013. The data analysis was conducted in August 2015.
Exposures  Maternal consumption of artificially sweetened beverages and sugar-sweetened beverages during pregnancy, determined by a food frequency questionnaire.
Main Outcomes and Measures  Infant BMI z score and risk of overweight at 1 year of age, determined from objective anthropometric measurements and defined according to World Health Organization reference standards.
Results  The mean (SD) age of the 3033 pregnant women was 32.4 (4.7) years, and their mean (SD) BMI was 24.8 (5.4). The mean (SD) infant BMI z score at 1 year of age was 0.19 (1.05), and 5.1% of infants were overweight. More than a quarter of women (29.5%) consumed artificially sweetened beverages during pregnancy, including 5.1% who reported daily consumption. Compared with no consumption, daily consumption of artificially sweetened beverages was associated with a 0.20-unit increase in infant BMI z score (adjusted 95% CI, 0.02-0.38) and a 2-fold higher risk of infant overweight at 1 year of age (adjusted odds ratio, 2.19; 95% CI, 1.23-3.88). These effects were not explained by maternal BMI, diet quality, total energy intake, or other obesity risk factors. There were no comparable associations for sugar-sweetened beverages.
Conclusions and Relevance  To our knowledge, we provide the first human evidence that maternal consumption of artificial sweeteners during pregnancy may influence infant BMI. Given the current epidemic of childhood obesity and widespread use of artificial sweeteners, further research is warranted to confirm our findings and investigate the underlying biological mechanisms, with the ultimate goal of informing evidence-based dietary recommendations for pregnant women."



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Bisphenol A in low doses can affect the reproductive system , obesity, and behaviour

"If rats are exposed to bisphenol A in low doses during early development it can lead to reduced sperm count, obesity and changes to breast development and behaviour. These are some of the findings of a new study from the National Food Institute, Technical University of Denmark. The results support previous animal studies, which have shown that low doses of bisphenol A can affect development of the metabolism as well as the reproductive and nervous systems."



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Antiobesity effect of Pediococcus pentosaceus LP28 on overweight subjects: a randomized, double-blind, placebo-controlled clinical trial : European Journal of Clinical Nutrition

Background/Objectives:
The population of the obese is increasing worldwide. Prevention and improvement of obesity are indispensable for decreasing the risk of metabolic disorders. We have recently shown that obesity and fatty liver are reduced by a plant-derived lactic acid bacterium, Pediococcus pentosaceus LP28 (LP28), in high-fat diet-induced obese mice. The aim of the present clinical study is to prove that LP28 is effective for reducing body fat and body weight, as shown in the experiment using mice.

Subjects/Methods:

The clinical trial was carried out as a double-blind, randomized, placebo-controlled study comprising 62 subjects (20–70 years of age, BMI 25–30 kg/m2). These subjects were randomly assigned to three groups that received living LP28, heat-killed LP28 or a placebo powder, administered orally once a day for 12 weeks.

Results:

Heat-killed LP28 reduced BMI (0.45 kg/m2, 95% CI (0.04, 0.86), P=0.035), body fat percentage (1.11%, (0.39, 1.82), P=0.002), body fat mass (1.17 kg (0.43, 1.92), P=0.004) and waist circumference (2.84 cm (0.74, 4.93), P=0.009) when compared with a placebo group. Fasting plasma glucose, HbA1c, fasting insulin, HOMA-IR and serum lipids levels did not change by either living LP28 or heat-killed LP28 intake.

Conclusions:

Heat-killed LP28 displays an antiobesity effect that reduces BMI, body fat and waist circumference, suggesting that the plant-derived lactic acid bacterium LP28 would be a promising preventive of metabolic syndrome."



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Epigenetic germline inheritance of diet-induced obesity and insulin resistance : Nature Genetics : Nature Publishing Group

"There is considerable controversy regarding epigenetic inheritance in mammalian gametes. Using in vitro fertilization to ensure exclusive inheritance via the gametes, we show that a parental high-fat diet renders offspring more susceptible to developing obesity and diabetes in a sex- and parent of origin–specific mode. The epigenetic inheritance of acquired metabolic disorders may contribute to the current obesity and diabetes pandemic."



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How a food packaging chemical could lead to weight gain - Medical News Today

"Martin von Bergen, head of the Department of Molecular Systems Biology at the Helmholtz Centre for Environmental Research (UFZ) in Germany, and colleagues found that the chemical di-(2-ethylhexyl)-phthalate (DEHP) led to a hormone imbalance in female mice that triggered weight gain, even when exposed to the chemical in low concentrations."

Physical activity and genetic predisposition to obesity in a multiethnic longitudinal study. - PubMed - NCBI

Physical activity (PA) has been shown to reduce the impact of FTO variation and obesity genetic risk scores (GRS) on BMI. We examined this interaction using a quantitative measure of PA and two adiposity indexes in a longitudinal multi-ethnic study. We analyzed the impact of PA on the association between 14 obesity predisposing variants (analyzed independently and as a GRS) and baseline/follow-up obesity measures in the multi-ethnic prospective cohort EpiDREAM (17423 participants from six ethnic groups). PA was analyzed using basic (low-moderate-high) and quantitative measures (metabolic equivalents (METS)), while BMI and the body adiposity index (BAI) were used to measure obesity. Increased PA was associated with decreased BMI/BAI at baseline/follow-up. FTO rs1421085, CDKAL1 rs2206734, TNNl3K rs1514176, GIPR rs11671664 and the GRS were associated with obesity measures at baseline and/or follow-up. Risk alleles of three SNPs displayed nominal associations with increased (NTRK2 rs1211166, BDNF rs1401635) or decreased (NPC1 rs1805081) basic PA score independently of BMI/BAI. Both basic and quantitative PA measures attenuated the association between FTO rs1421085 risk allele and BMI/BAI at baseline and follow-up. Our results show that physical activity can blunt the genetic effect of FTO rs1421085 on adiposity by 36-75% in a longitudinal multi-ethnic cohort.

Gut microbes signal to the brain when they are full

"Don't have room for dessert? The bacteria in your gut may be telling you something. Twenty minutes after a meal, gut microbes produce proteins that can suppress food intake in animals, reports a study published November 24 (here in Cell Metabolism. )The researchers also show how these proteins injected into mice and rats act on the brain reducing appetite, suggesting that gut bacteria may help control when and how much we eat."



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