Metabolic Syndrome: Focus on Dyslipidemia

Ginsberg, Henry N.; Zhang, Yuanli; Hernandez‐Ono, Antonio

doi:10.1038/oby.2006.281

Cited by 193 publications

(141 citation statements)

References 67 publications

(57 reference statements)

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“…Also, dysregulation of lipid metabolism has been identified as a critical contributor to the mechanistic etiology of insulin resistance (Ginsberg et al ., 2006). Control mice fed HFD had increased total plasma cholesterol levels when compared to control and Ames dwarf mice fed STD ( P < 0.003) (Fig.…”

Section: Resultsmentioning

confidence: 99%

Long‐lived hypopituitary Ames dwarf mice are resistant to the detrimental effects of high‐fat diet on metabolic function and energy expenditure

Hill

Fang

Miquet³

et al. 2016

Aging Cell

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SummaryGrowth hormone (GH) signaling stimulates the production of IGF‐1; however, increased GH signaling may induce insulin resistance and can reduce life expectancy in both mice and humans. Interestingly, disruption of GH signaling by reducing plasma GH levels significantly improves health span and extends lifespan in mice, as observed in Ames dwarf mice. In addition, these mice have increased adiposity, yet are more insulin sensitive compared to control mice. Metabolic stressors such as high‐fat diet (HFD) promote obesity and may alter longevity through the GH signaling pathway. Therefore, our objective was to investigate the effects of a HFD (metabolic stressor) on genetic mechanisms that regulate metabolism during aging. We show that Ames dwarf mice fed HFD for 12 weeks had an increase in subcutaneous and visceral adiposity as a result of diet‐induced obesity, yet are more insulin sensitive and have higher levels of adiponectin compared to control mice fed HFD. Furthermore, energy expenditure was higher in Ames dwarf mice fed HFD than in control mice fed HFD. Additionally, we show that transplant of epididymal white adipose tissue (eWAT) from Ames dwarf mice fed HFD into control mice fed HFD improves their insulin sensitivity. We conclude that Ames dwarf mice are resistant to the detrimental metabolic effects of HFD and that visceral adipose tissue of Ames dwarf mice improves insulin sensitivity in control mice fed HFD.

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Section: Resultsmentioning

confidence: 99%

Long‐lived hypopituitary Ames dwarf mice are resistant to the detrimental effects of high‐fat diet on metabolic function and energy expenditure

Hill

Fang

Miquet³

et al. 2016

Aging Cell

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“…Reliable biomarkers for insulin resistance that can be measured in nonfasting blood samples may therefore prove to be of significant clinical value for early identification of at-risk individuals. Early identification is important, since a substantial part of patients with type 2 diabetes already have diabetic complications at the time of diagnosis [19,20]. We have previously shown that high levels of sCD163 in the general population carry a large increased risk of later development of type 2 diabetes [13], but whether this is linked to insulin resistance is not known.…”

Section: Discussionmentioning

confidence: 99%

Soluble CD163: a biomarker linking macrophages and insulin resistance

et al. 2012

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Aims/hypothesis Soluble CD163 (sCD163) was recently identified as a strong risk marker for developing type 2 diabetes. We hypothesised that sCD163 independently associates with insulin resistance. Methods This cross-sectional study includes 234 participants: 96 with type 2 diabetes, 34 with impaired glucose tolerance (IGT) and 104 with normal glucose tolerance (NGT), matched for sex and BMI. Glucose-lowering medication was paused for 1 week before plasma samples were obtained for determination of sCD163 and other inflammatory and metabolic variables. Insulin resistance was estimated by homeostasis model assessment of insulin resistance (HOMA-IR).

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“…Metabolic syndrome contributes to chronic heart disease, atherosclerosis, T2DM, and NAFLD. Dyslipidemia causes insulin resistance and inflammation, and pathogenesis of NAFLD (Ginsberg et al, 2006;Cohen et al, 2011). NAFLD is a spectrum of chronic liver abnormalities from simple steatosis to NASH to liver cirrhosis (Yeh and Brunt, 2007).…”

Section: Fatty Liver Disease Diabetes and Obesitymentioning

confidence: 99%