A workshop was organized by the National Institute of Environmental Health Sciences (NIEHS) Division of the National Toxicology Program (NTP) to assess whether and how exposure to environmental chemicals contribute to obesity and diabetes. A group of more than 50 scientists from various medical fields such as endocrinology, toxicology, epidemiology, bioinformatics and other experts participated in the evaluation of current literature.
The lead reviewers of the workshop were Kristina A. Thayer, Jerrold J. Heindel, John R. Bucher, Michael A. Gallo. The workshop focused on the adverse effects of arsenic, maternal smoking/nicotine, organotins, bisphenol A (BPA), persistent organic pollutants (POPs), pesticides and phthalates on the health of humans and experimental animals. The prime objective of the workshop was to formulate and forward recommendations for a research program after a critical analysis of the environmental chemicals.
In order to assess the potential cellular pathways and hypothesize how certain chemicals might hamper the biological processes concerned with diabetes and obesity, high screening data from Tox21 were taken into account.
Existing literature suggested that type-2 diabetes was affected by several environmental chemicals. The hypothesis of ‘developmental obesogen’ was also supported. The hypothesis suggests that exposure to certain chemicals may alter human metabolism and lead to obesity.
Maternal Smoking and Nicotine: An important finding of the workshop was that nicotine is a strong ‘developmental obesogen’ in human beings.
Arsenic: An association was found between diabetes and arsenic in people from high-arsenic exposure regions such as Taiwan and Bangladesh.
Organotins: No epidemiological studies of organotin exposure and obesity or diabetes were identified during the literature search.
POPs: Certain POPs such as DDT, DDD, and polychlorinated biphenyl (PCBs) showed positive association with diabetes.
Phthalates: Hatch et al studied the exposure of phthalates on diabetes and obesity. The urinary phthalate metabolite monoethyl phthalate was the common phthalate metabolite associated with high body mass index (BMI).
BPA: One pilot study suggests that bisphenol-A (BPA) pose a potential risk for childhood obesity. BPA affects insulin release, glucose homeostasis, adipogenesis and cellular signaling in pancreatic β cells. Pesticides: Pesticide acts as an important risk factor of obesity and diabetes.
It is observed that the environmental chemical exposure produces more prominent effects when combined with high-carbohydrate, high-fat or high-calorie diet.
The workshop concluded on the hope that further researches would be done internationally to better understand the impact of environmental pollutants on the prevalence of obesity, metabolic syndrome and diabetes.
The report highlights the need of further research and analysis regarding specific exposures of environmental chemicals and their outcome.
Reference: Role of Environmental Chemicals in Diabetes and Obesity; Kristina et al; Environmental Health Prospectives 2012.
The lead reviewers of the workshop were Kristina A. Thayer, Jerrold J. Heindel, John R. Bucher, Michael A. Gallo. The workshop focused on the adverse effects of arsenic, maternal smoking/nicotine, organotins, bisphenol A (BPA), persistent organic pollutants (POPs), pesticides and phthalates on the health of humans and experimental animals. The prime objective of the workshop was to formulate and forward recommendations for a research program after a critical analysis of the environmental chemicals.
In order to assess the potential cellular pathways and hypothesize how certain chemicals might hamper the biological processes concerned with diabetes and obesity, high screening data from Tox21 were taken into account.
Existing literature suggested that type-2 diabetes was affected by several environmental chemicals. The hypothesis of ‘developmental obesogen’ was also supported. The hypothesis suggests that exposure to certain chemicals may alter human metabolism and lead to obesity.
Maternal Smoking and Nicotine: An important finding of the workshop was that nicotine is a strong ‘developmental obesogen’ in human beings.
Arsenic: An association was found between diabetes and arsenic in people from high-arsenic exposure regions such as Taiwan and Bangladesh.
Organotins: No epidemiological studies of organotin exposure and obesity or diabetes were identified during the literature search.
POPs: Certain POPs such as DDT, DDD, and polychlorinated biphenyl (PCBs) showed positive association with diabetes.
Phthalates: Hatch et al studied the exposure of phthalates on diabetes and obesity. The urinary phthalate metabolite monoethyl phthalate was the common phthalate metabolite associated with high body mass index (BMI).
BPA: One pilot study suggests that bisphenol-A (BPA) pose a potential risk for childhood obesity. BPA affects insulin release, glucose homeostasis, adipogenesis and cellular signaling in pancreatic β cells. Pesticides: Pesticide acts as an important risk factor of obesity and diabetes.
It is observed that the environmental chemical exposure produces more prominent effects when combined with high-carbohydrate, high-fat or high-calorie diet.
The workshop concluded on the hope that further researches would be done internationally to better understand the impact of environmental pollutants on the prevalence of obesity, metabolic syndrome and diabetes.
The report highlights the need of further research and analysis regarding specific exposures of environmental chemicals and their outcome.
Reference: Role of Environmental Chemicals in Diabetes and Obesity; Kristina et al; Environmental Health Prospectives 2012.
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