We investigated the association of systemic and local tissue stress responses with heat-tolerant (TOL) levels in mice. Thirty-eight mice were assigned into control and three heat exposure groups-TOL, moderately tolerant, and intolerant (INT), based on their overall thermal responses. Real-time core temperature, blood pressure, and heart rate (HR) were assessed during heat exposure (39.5 °C) under conscious condition. Tissue samples were collected 18-22 h following heat exposure. INT mice had significantly higher peak mean arterial pressure and HR than TOL mice during heat exposure. Plasma corticosterone levels were significantly higher in INT than in control mice. No significant changes in plasma cytokines or markers of oxidative status were observed. INT mice showed significant increases in HSP72 and HSP90 protein and mRNA levels in liver, heart, and gastrocnemius muscles compared to TOL and control mice. In contrast, INT mice had significantly lower heat shock factor 1 and glucocorticoid receptor protein and mRNA levels in these tissues than TOL and control mice. These results indicate that acute heat exposure induces stress responses in various tissues of INT mice, but not TOL mice. Upregulation of stress proteins by acute heat exposure involves both transcriptional and translational pathways.
Although progress has been made to understand the association between physiological and lifestyle behaviors with regard to obesity, ethnic differences in markers of obesity and pathways towards obesity remain somewhat unexplained. However, obesity remains a serious growing concern. This paper highlights ethnic differences in African Americans and Caucasians that may contribute to the higher prevalence of obesity among African Americans. Understanding ethnic differences in metabolic syndrome criteria, functioning of the hypothalamic pituitary adrenal axis, variations in glucocorticoid sensitivity and insulin resistance, and physical activity and cardiovascular fitness levels may help to inform practical clinical and public health interventions and reduce obesity disparities.
Background: Obesity is a modifiable risk factor for hypertension and T2D. Objective(s) : We examined relations between fasting plasma adiponectin (ADIP), C-reactive protein (CRP) concentrations and markers of T2D in African Americans (AA).
Oxidative stress and cellular injury have been implicated in induction of HSP72 by alcohol. We investigated the association between HSP72 induction and oxidative stress in mouse tissues following short-term administration of high doses of alcohol and caffeine alone or in combination. Adult male C57BL/6J mice were gavaged with vehicle, alcohol (∼1.7 g/kg/day), caffeine (∼44 mg/kg/day), or alcohol plus caffeine once daily for ten consecutive days. Upon completion of the treatments, tissues were collected for structural and biochemical analyses. Alcohol alone caused mild to moderate lesions in heart, liver, and gastrocnemius muscle. Similar structural changes were observed following administration of alcohol and caffeine combined. Alcohol administration also led to decreased glutathione levels in all three tissues and reduced plasma superoxide dismutase capacity. In contrast, alcohol and caffeine in combination reduced glutathione levels only in liver and gastrocnemius muscle and had no effect on plasma superoxide dismutase. Significant elevations in HSP72 protein and mRNA and in HSF1 protein levels were noted only in liver by alcohol alone or in combination with caffeine. No significant changes in morphology and HSP72 were detected in any tissues tested following administration of caffeine alone. These results suggest that a redox mechanism is involved in the structural impairment caused by short-term high-dose alcohol. Oxidative tissue injury by alcohol may not be associated with tissue HSP72 induction. Induction of HSP72 in liver by alcohol is mediated at both the transcriptional and translational levels.
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