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Fructose metabolism, cardiometabolic risk, and the epidemic of coronary artery disease.
Mirtschink, P, Jang, C, Arany, Z, Krek, W
European heart journal. 2018;(26):2497-2505
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Abstract
Despite strong indications that increased consumption of added sugars correlates with greater risks of developing cardiometabolic syndrome (CMS) and cardiovascular disease (CVD), independent of the caloric intake, the worldwide sugar consumption remains high. In considering the negative health impact of overconsumption of dietary sugars, increased attention is recently being given to the role of the fructose component of high-sugar foods in driving CMS. The primary organs capable of metabolizing fructose include liver, small intestine, and kidneys. In these organs, fructose metabolism is initiated by ketohexokinase (KHK) isoform C of the central fructose-metabolizing enzyme KHK. Emerging data suggest that this tissue restriction of fructose metabolism can be rescinded in oxygen-deprived environments. In this review, we highlight recent progress in understanding how fructose metabolism contributes to the development of major systemic pathologies that cooperatively promote CMS and CVD, reference recent insights into microenvironmental control of fructose metabolism under stress conditions and discuss how this understanding is shaping preventive actions and therapeutic approaches.
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[Efficacy of hypobaric hypoxia in the treatment of arterial hypertension in postmenopausal women].
Tin'kov, AN, Konstantinova, OD, Kshniaseva, SK
Terapevticheskii arkhiv. 2011;(12):16-9
Abstract
AIM: To assess efficacy of adaptation to periodic hypobaric hypoxia (PHH) in the treatment of postmenopausal women with arterial hypertension (AH). MATERIAL AND METHODS The method of adaptation to PHH in the pressure chamber Ural-1 (22 three-hour daily sessions, pressure 460 mmHg) was used in 46 postmenopausal AH women (mean age 53.8 +/- 3.9 years). The method was assessed for effects on blood pressure (BP), symptoms of menopausal syndrome, body mass, levels of some hormones, lipid and carbohydrate metabolism. RESULTS Adaptation to PHH reduced systolic pressure by 13.9%, diastolic one--by 8.2%, the levels of follicule stimulating and luteinising hormones by 26.8 and 21.5%, respectively, cholesterol--by 14.7, glucose--by 21.3, insulin--20.2%; estradiol and dehydroepiandrosteron sulphate concentrations rose by 19.3 and 15.2%, respectively. CONCLUSION Adaptation to PHH produced an antihypertensive effect and a positive trend in clinicometabolic indices in AH women in postmenopause.