Key result
Exercise training plus caloric restriction raises cardiac eNOS but fails to preserve cardioprotective oxytocin-NP signaling.
Why the study?
Does combined exercise training and caloric restriction improve the cardiac oxytocin-natriuretic peptide system in diabetic mice?
Does combined exercise training and caloric restriction improve the cardiac oxytocin-natriuretic peptide system in diabetic mice?
Answers are grounded in this paper and cite their sources.
BACKGROUND: Regular exercise training (ET) and caloric restriction (CR) are the frontline strategies in the treatment of type 2 diabetes mellitus with the aim at reducing cardiometabolic risk. ET and CR improve body weight and glycemic control, and experimental studies indicate that these paradigms afford cardioprotection. In this study, the effects of combined ET and CR on the cardioprotective oxytocin (OT)-natriuretic peptide (NP) system were determined in the db/db mouse, a model of type 2 diabetes associated with insulin resistance, hyperglycemia, and obesity. METHODS: Five-week-old male db/db mice were assigned to the following groups: sedentary, ET, and ET + CR. Nonobese heterozygote littermates served as controls. ET was performed on a treadmill at moderate intensity, and CR was induced by reducing food intake by 30% of that consumed by sedentary db/db mice for a period of 8 weeks. RESULTS: After 8 weeks, only ET + CR, but not ET, slightly improved body weight compared to sedentary db/db mice. Regardless of the treatment, db/db mice remained hyperglycemic. Hearts from db/db mice demonstrated reduced expression of genes linked to the cardiac OT-NP system. In fact, compared to control mice, mRNA expression of GATA binding protein 4 (GATA4), OT receptor, OT, brain NP, NP receptor type C, and endothelial nitric oxide synthase (eNOS) was decreased in hearts from sedentary db/db mice. Both ET alone and ET + CR increased the mRNA expression of GATA4 compared to sedentary db/db mice. Only ET combined with CR produced increased eNOS mRNA and protein expression. CONCLUSION: Our data indicate that enhancement of eNOS by combined ET and CR may improve coronary endothelial vasodilator dysfunction in type 2 diabetes but did not prevent the downregulation of cardiac expression in the OT-NP system, possibly resulting from the sustained hyperglycemia and obesity in diabetic mice.
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Broderick et al. (2017) studied Type 2 Diabetes Mellitus. Exercise training and caloric restriction vs. Sedentary db/db mice was evaluated on Cardiac oxytocin-natriuretic peptide system gene and protein expression (including eNOS and GATA4) (p=<0.05). Combined exercise training and caloric restriction for 8 weeks increased cardiac eNOS expression but failed to prevent the overall downregulation of the cardioprotective oxytocin-natriuretic peptide system in diabetic mice.
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