Kato et al_FigS2

This file include data for Figure S2

Kato et al_Fig1

This file include data for Figure 1. We estimated the correlations between body weight (BW) on postnatal day (PND) 0 and subsequent BWs to clarify the long-term effect of birth weight on their development

Kato et al_FigS1

This file include data for Figure S1. This figure shows the torpor expression in female mice we tested

Kato et al_Fig4

This file include data for Figure 4

Kato et al_torpor bout length

We calculated the length of torpor expression using a formula described in this file

Kato et al_logger weight

Kato et al_logger weigh

Kato et al_FigS3

This file include data for Figure S3. This figure shows the torpor expression in male mice we tested

Kato et al_Fig2

This file include data for Figure 2. The figure shows four unique body temperature patterns and torpor expression induced by fasting

Kato et al_bodyweight

This file include body weight data from 114 mice (10 litters). Each sheet include actual bodyweight data, relative body weight data and body weight immediately before fasting in torpor induction trials, respectively

Altered glucose metabolism and hypoxic response in alloxan-induced diabetic atherosclerosis in rabbits

<div><p>Diabetes mellitus accelerates atherosclerosis that causes most cardiovascular events. Several metabolic pathways are considered to contribute to the development of atherosclerosis, but comprehensive metabolic alterations to atherosclerotic arterial cells remain unknown. The present study investigated metabolic changes and their relationship to vascular histopathological changes in the atherosclerotic arteries of rabbits with alloxan-induced diabetes. Diabetic atherosclerosis was induced in rabbit ilio-femoral arteries by injecting alloxan (100 mg/kg), injuring the arteries using a balloon, and feeding with a 0.5% cholesterol diet. We histologically assessed the atherosclerotic lesion development, cellular content, pimonidazole positive-hypoxic area, the nuclear localization of hypoxia-inducible factor-1α, and apoptosis. We evaluated comprehensive arterial metabolism by performing metabolomic analyses using capillary electrophoresis-time of flight mass spectrometry. We evaluated glucose uptake and its relationship to vascular hypoxia using ¹⁸F-fluorodeoxyglucose and pimonidazole. Plaque burden, macrophage content, and hypoxic areas were more prevalent in arteries with diabetic, than non-diabetic atherosclerosis. Metabolomic analyses highlighted 12 metabolites that were significantly altered between diabetic and non-diabetic atherosclerosis. A half of them were associated with glycolysis metabolites, and their levels were decreased in diabetic atherosclerosis. The uptake of glucose evaluated as ¹⁸F-fluorodeoxyglucose in atherosclerotic lesions increased according to increased macrophage content or hypoxic areas in non-diabetic, but not diabetic rabbits. Despite profound hypoxic areas, the nuclear localization of hypoxia-inducible factor-1α decreased and the number of apoptotic cells increased in diabetic atherosclerotic lesions. Altered glycolysis metabolism and an impaired response to hypoxia in atherosclerotic lesions under conditions of insulin-dependent diabetes might be involved in the development of diabetic atherosclerosis.</p></div