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1. Psychosocial stress is reported to be one of the main causes of obesity. Based on observations in studies that relate stress and gut inflammation to obesity, the present study hypothesized that chronic stress, via inflammation, alters the expression of nutrient transporters and contributes to the development of metabolic syndrome.2. Rats were exposed to restraint stress for 4 h/day for 5 days/week for eight consecutive weeks. Different segments of rat intestine were then collected and analysed for signs of pathophysiological changes and the expression of Niemann-Pick C1-like-1 (NPC1L1), sodium-dependent glucose transporter-1 (SLC5A1, previously known asSGLT1) and facilitative glucose transporter-2 (SLC2A2, previously known asGLUT2). In a separate experiment, the total anti-oxidant activity (TAA)–time profile of control isolated intestinal segments was measured.3. Stress decreased the expression ofNPC1L1in the ileum and upregulatedSLC5A1in both the jejunum and ileum andSLC2A2in the duodenum. Inflammation and morphological changes were observed in the proximal region of the intestine of stressed animals. Compared with jejunal and ileal segments, the rate of increase in TAA was higher in the duodenum, indicating that the segment contained less anti-oxidants; anti-oxidants may function to protect the tissues.4. In conclusion, stress alters the expression of hexose and lipid transporters in the gut. The site-specific increase in the expression ofSLC5A1andSLC2A2may be correlated with pathological changes in the intestine. The ileum may be protected, in part, by gut anti-oxidants. Collectively, the data suggest that apart from causing inflammation, chronic stress may promote sugar uptake and contribute to hyperglycaemia.