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Role of vascular oxidative stress in obesity and metabolic syndrome.

Youn JY, Siu KL, Lob HE, Itani H, Harrison DG, Cai H - Diabetes (2014)

Bottom Line: Obesity is associated with vascular diseases that are often attributed to vascular oxidative stress.This was associated with development of glucose intolerance, reduced HDL cholesterol, and increased levels of leptin and MCP-1.In conclusion, these data indicate that vascular oxidative stress induces obesity and metabolic syndrome, accompanied by and likely due to exercise intolerance, vascular inflammation, and augmented adipogenesis.

View Article: PubMed Central - PubMed

Affiliation: Division of Molecular Medicine and Cardiology, Cardiovascular Research Laboratories, Departments of Anesthesiology and Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA.

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Related in: MedlinePlus

Changes in water intake, food intake, and energy intake in WT and tgsm/p22phox mice fed with control or high-fat diet for 6 weeks. A: Water intake was measured weekly, and there were no significant changes among the four different groups except for weeks 3–5. B: Weekly food intake was decreased in WT mice after high-fat feeding for 2 weeks. C: Energy intake was calculated into kilocalories from grams of food ingested as described in Research Design and Methods. Data are presented as mean ± SEM; n = 7–11 for A–C.
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Figure 2: Changes in water intake, food intake, and energy intake in WT and tgsm/p22phox mice fed with control or high-fat diet for 6 weeks. A: Water intake was measured weekly, and there were no significant changes among the four different groups except for weeks 3–5. B: Weekly food intake was decreased in WT mice after high-fat feeding for 2 weeks. C: Energy intake was calculated into kilocalories from grams of food ingested as described in Research Design and Methods. Data are presented as mean ± SEM; n = 7–11 for A–C.

Mentions: High-fat feeding induced a significantly greater increase in body weight in tgsm/p22phox mice compared with wild-type (WT) controls (Fig. 1A–B). The composition of the high-fat diet is provided in Supplementary Table 1. As shown in Supplementary Table 2, resting levels of body weight, food intake, water intake, energy intake, leptin, cholesterol, insulin, and glucose were not different among all groups. Figure 1A illustrates the appearance of representative WT or tgsm/p22phox mice fed a normal or high-fat diet for 6 weeks. Whereas body weight of 6-month-old WT mice increased from 30.81 ± 0.71 g to 37.89 ± 1.16 g after high-fat feeding for 6 weeks, body weight of tgsm/p22phox mice increased from 32.16 ± 2.34 g to 43.03 ± 1.44 g (Fig. 1B). The percentage of body weight increase was 34% vs. 23% for tgsm/p22phox vs. WT mice, indicating 50% more weight gain in the tgsm/p22phox animals. Of note, the augmented weight gain in tgsm/p22phox mice was accompanied by increased abdominal white fat (Fig. 1C) and liver size (Fig. 1D). There were no noticeable increases in intake of water, food, or calculated energy in tgsm/p22phox mice compared with WT controls when fed high-fat diet (Fig. 2A–C). Although water intake was transiently reduced in tgsm/p22phox mice at 3 weeks of high-fat feeding, it did not affect energy intake.


Role of vascular oxidative stress in obesity and metabolic syndrome.

Youn JY, Siu KL, Lob HE, Itani H, Harrison DG, Cai H - Diabetes (2014)

Changes in water intake, food intake, and energy intake in WT and tgsm/p22phox mice fed with control or high-fat diet for 6 weeks. A: Water intake was measured weekly, and there were no significant changes among the four different groups except for weeks 3–5. B: Weekly food intake was decreased in WT mice after high-fat feeding for 2 weeks. C: Energy intake was calculated into kilocalories from grams of food ingested as described in Research Design and Methods. Data are presented as mean ± SEM; n = 7–11 for A–C.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4066332&req=5

Figure 2: Changes in water intake, food intake, and energy intake in WT and tgsm/p22phox mice fed with control or high-fat diet for 6 weeks. A: Water intake was measured weekly, and there were no significant changes among the four different groups except for weeks 3–5. B: Weekly food intake was decreased in WT mice after high-fat feeding for 2 weeks. C: Energy intake was calculated into kilocalories from grams of food ingested as described in Research Design and Methods. Data are presented as mean ± SEM; n = 7–11 for A–C.
Mentions: High-fat feeding induced a significantly greater increase in body weight in tgsm/p22phox mice compared with wild-type (WT) controls (Fig. 1A–B). The composition of the high-fat diet is provided in Supplementary Table 1. As shown in Supplementary Table 2, resting levels of body weight, food intake, water intake, energy intake, leptin, cholesterol, insulin, and glucose were not different among all groups. Figure 1A illustrates the appearance of representative WT or tgsm/p22phox mice fed a normal or high-fat diet for 6 weeks. Whereas body weight of 6-month-old WT mice increased from 30.81 ± 0.71 g to 37.89 ± 1.16 g after high-fat feeding for 6 weeks, body weight of tgsm/p22phox mice increased from 32.16 ± 2.34 g to 43.03 ± 1.44 g (Fig. 1B). The percentage of body weight increase was 34% vs. 23% for tgsm/p22phox vs. WT mice, indicating 50% more weight gain in the tgsm/p22phox animals. Of note, the augmented weight gain in tgsm/p22phox mice was accompanied by increased abdominal white fat (Fig. 1C) and liver size (Fig. 1D). There were no noticeable increases in intake of water, food, or calculated energy in tgsm/p22phox mice compared with WT controls when fed high-fat diet (Fig. 2A–C). Although water intake was transiently reduced in tgsm/p22phox mice at 3 weeks of high-fat feeding, it did not affect energy intake.

Bottom Line: Obesity is associated with vascular diseases that are often attributed to vascular oxidative stress.This was associated with development of glucose intolerance, reduced HDL cholesterol, and increased levels of leptin and MCP-1.In conclusion, these data indicate that vascular oxidative stress induces obesity and metabolic syndrome, accompanied by and likely due to exercise intolerance, vascular inflammation, and augmented adipogenesis.

View Article: PubMed Central - PubMed

Affiliation: Division of Molecular Medicine and Cardiology, Cardiovascular Research Laboratories, Departments of Anesthesiology and Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA.

Show MeSH
Related in: MedlinePlus