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Lifelong consumption of low-dosed food pollutants and metabolic health
  1. Brigitte Le Magueresse-Battistoni,
  2. Hubert Vidal,
  3. Danielle Naville
  1. Laboratoire de Recherche en Cardiovasculaire, Métabolisme, Diabétologie et Nutrition, CarMeN INSERM U1060, Lyon-1 University, INRA UMR1397, INSA-Lyon, Lyon, France
  1. Correspondence to Dr Brigitte Le Magueresse-Battistoni, Laboratoire de Recherche en Cardiovasculaire, Métabolisme, Diabétologie et Nutrition, CarMeN INSERM U1060/UMR INRA 1397/Université Lyon1, Faculté de Médecine Lyon-sud-BP12, Secteur 1, 165 Chemin du Grand Revoyet, 69921 OULLINS Cedex, Lyon, France; Brigitte.lemagueresse{at}inserm.fr

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Obesity is a major public health problem because it is a risk factor for metabolic disorders including type 2 diabetes and cardiovascular disorders. Its evolution is pandemic with more than 1.4 billion adults overweight in 2008, and the WHO predicts that by 2015 about 700 million people will be obese. Nowadays, an estimate of 347 million people worldwide has diabetes, and diabetes is projected to be the seventh leading cause of death in 2030.1 In addition, diabetes has a heavy cost on the economy and quality of life. For example, the total estimated cost of diagnosed diabetes in 2012 in the USA was $245 billion.2 Type 2 diabetes results from the body's ineffective use of insulin, a hypoglycaemic hormone secreted by the pancreas that plays a major metabolic role in maintaining blood glucose levels in the normal range. The first step leading to diabetes is insulin resistance that develops in the metabolically active tissues (ie, liver, skeletal muscle and adipose tissues) and eventually leads to the classic triad of hyperinsulinaemia, hyperglycaemia and hypertriglyceridaemia, which are the characteristic features of type 2 diabetes.3

Obesity is a multifactorial disease in which, besides genetic predisposition, excessive food intake combined with physical inactivity has generally been implicated. However, it was recently suggested that food pollutants could contribute to the aetiology of obesity and type 2 diabetes.4 This hypnothesis is based on several findings including the speed with which the incidence of obesity and its related metabolic disorders increases that excludes the only involvement of genetic factors and strengthens the environmental origin hypothesis. Furthermore, the production and usage of synthetic chemicals that have paralleled the incidence of diabetes5 support the hypothesis that the exposure to chemicals may have damaged physiological mechanisms regulating glucose and lipid metabolism.6 This assumption is …

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