Metabolic consequences of chronic intermittent mild stress exposure

Abstract

Chronic stress in humans has divergent effects on food intake, with some individuals reporting increased vs. decreased food intake during stress. This divergence may depend in part on stress intensity, with higher-intensity stressors preferentially promoting anorexia. Consistent with this idea, rodents given a high-intensity chronic variable stress paradigm have robustly decreased food intake and body weight gain. However, the metabolic effects of a less intense chronic stress paradigm are not clear. Thus in the present study, adult male rats were given chronic intermittent mild stress (CIMS) exposure (3 cycles, in which each cycle consists of once daily mild stress for 5 days/week for 2 weeks, followed by 2 weeks of no stress) vs. non-stress controls, combined with ongoing access to a palatable diet (PD; choice of chow, high-fat diet, 30% sucrose drink, and water) vs. control diet (chow and water). As expected, access to PD increased caloric intake, body weight gain, and adiposity, and impaired glucose tolerance. CIMS decreased body weight gain only during the first cycle of stress and did not affect body weight gain thereafter, regardless of diet. Moreover, CIMS did not alter total food intake, adiposity or glucose tolerance regardless of diet. Lastly, CIMS transiently increased high-fat diet preference in PD-fed rats during the first stress cycle. Collectively, these results suggest that CIMS has relatively modest metabolic effects that occur primarily during initial stress exposure. These results support the hypothesis that the metabolic consequences of chronic stress vary with stress intensity and/or frequency.

Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress

“…This state did not affect GR gene expression, as revealed in this and our previous study, but rather led to activation and nuclear accumulation of GR [44]. In addition, chronic stress per se did not alter glucose homeostasis, which is in line with previous reports that chronic mild stress has relatively modest effects on glucose homeostasis that occurs primarily at the beginning of stress exposure [45]. On the other hand, fructose-fed unstressed animals displayed altered glucose homeostasis, as characterized by hypoglycemia, hyperinsulinemia and impaired glucose tolerance, as revealed by IPGTT.…”

The Dichotomous Effect of Chronic Stress on Obesity

“…Models characterized by low to mild challenge such as exposure to open field, result in BAT-independent thermogenesis ineffectual for modulating energy balance [91]. Similarly, an intermittent version of the chronic mild stress model exerted minimal and transient effects on energy balance [92]. Exposing mice to intermitted cold resulted in increased adiposity in the absence of reported increase in thermogenesis or BAT recruitment/activation [38].…”

From covalent bonds to eco-physiological pharmacology of secondary plant metabolites

“…Such molecules are well-known for their anti-obesity and other therapeutically interesting properties [117; 118], and their modulatory effects on cognitive processes involved in eating behavior [119; 120]. The link between homeostatic stress responses and metabolic diseases is well known [121,122] acids are pharmacologically, toxicologically, and clinically the most extensively studied [139; 140; 141; 142],. Their daily consumption can lead to marked differences in gut microbial ecology observed in different human population [143; 144; 145] that can also modulate physiological stress responses [146].…”