Social stress, obesity and glucose tolerance: a psychobiological investigation

Social stress, obesity and glucose tolerance: a psychobiological investigation Stress has been associated with changes in eating behavior and food preferences (Dallman et al. 2003). In humans psychosocial and socio-economical challenges have been related with neuroendocrine-autonomic dysregulation followed by visceral obesity and increased in body mass index (BMI) (Van Strien et al. 1986, Rosmond, Dallman and Björntorp 1998). The chronic activation of stress response system, leads to an increase in food intake, especially high palatable food (Dallman et al. 2004, Dallman et al. 2005), obesity and metabolic syndrome (Rosmond et al. 1998, Björntorp 1993, Björntorp 1996a, Tsigos and Chrousos 2002). Altogether these metabolic disorders result in a pre-diabetic state, which may turn in type 2 diabetes (T2D) in susceptible individuals in a nutrional rich environment (Björntorp 1996b, Boden 2002, Chan et al. 1994, Colditz et al. 1990, DeFronzo 2004). In addition, comorbid pathology such as “atypical depression” linked to stress (DSM-IV, American Psychiatric Association, 2000) has been associated to eating disorders-induced obesity.(Mitchell and Mussell 1995, Stein et al. 2007, Stunkard 2011). While several genetic or pharmacological animal models of metabolic syndrome and T2D have been developed, so far there is a paucity of models in which the diseases are triggered by psychogenic stimuli. Aim of the present study is: Chapter One: the original characterization of a mouse models of early metabolic syndrome/T2D onset induced by exposing mice to chronic subordination stress in the presence of high fat diet. Chapter Two: determine if vulnerability to stress induced metabolic disease is status dependent. Specifically we will directly compare the metabolic consequences of being high in rank (dominant) and low in rank (subordinate) in mice exposed to our model of chronic psychosocial stress CPS and HFD Chapter Three: characterized if CPS may be considered a model of stress- induced binge eating disorders (BED) and understand the role of hyperphagia in stressed-induced obesity and T2D using a Pair-feeding protocol.