Overproduction of altered VLDL in an insulin-resistance rat model: Influence of SREBP-1c and PPAR-α

Lucero, Diego; Miksztowicz, Verónica; Macri, Elisa Vanesa; López, Gustavo; Friedman, Sílvia; Berg, Gabriela; Zago, Valeria; Schreier, Laura

doi:10.1016/j.arteri.2014.11.002

Cited by 20 publications

(15 citation statements)

References 30 publications

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“…The increase in VLDL-C upregulates SREBP-1c mRNA gene expression and subsequently downregulates PPAR-α mRNA gene expression (Lucero et al 2015). In this study, HFD increased mRNA expression of SREBP-1c, and AGM treatment inhibited this increase.…”

Section: Discussionmentioning

confidence: 73%

Attenuation of insulin resistance in rats by agmatine: role of SREBP-1c, mTOR and GLUT-2

Sharawy

El‐Awady

Megahed

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Insulin resistance is a serious health condition worldwide; however, its exact mechanisms are still unclear. This study investigates agmatine (AGM; an endogenous metabolite of L-arginine) effects on insulin resistance induced by high fructose diet (HFD) in rats and the possible involved mechanisms. Sprague Dawley rats were fed 60% HFD for 12 weeks, and AGM (10 mg/kg/day, orally) was given from week 9 to 12. AGM significantly reduced HFD-induced elevation in fasting insulin level, homeostasis model assessment of insulin resistance (HOMA-IR) index and liver glycogen content from 3.44-, 3.62- and 2.07- to 2.59-, 2.78- and 1.3-fold, respectively, compared to the control group, while it increased HFD-induced reduction in glucose tolerance. Additionally, AGM significantly decreased HFD-induced elevation in serum triglycerides, low density lipoprotein cholesterol and very low density lipoprotein cholesterol levels from 3.18-, 2.97- and 4.75- to 1.25-, 1.25- and 1.07-fold, respectively, compared to control group. Conversely, AGM had no significant effect on HFD-induced changes in fasting glucose, glycosylated hemoglobin, insulin tolerance and high density lipoprotein cholesterol. Furthermore, AGM significantly reduced HFD-induced elevation in mRNA expression of glucose transporter type-2 (GLUT-2), mammalian target of rapamycin (mTOR) and sterol regulatory element-binding protein-1c (SREBP-1c) without affecting that of peroxisome proliferator-activated receptor-alpha (PPAR-α) in the liver. Additionally, AGM enhanced ACh-induced aortic relaxation and attenuated liver steatosis induced by HFD. In conclusion, AGM may have a therapeutic potential in insulin resistance through suppressing SREBP-1c, mTOR and GLUT-2 in liver.

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Section: Discussionmentioning

confidence: 73%

Attenuation of insulin resistance in rats by agmatine: role of SREBP-1c, mTOR and GLUT-2

Sharawy

El‐Awady

Megahed

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

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“…TG/HDL-C was found to be closely associated with insulin resistance in different populations including Caucasians, Korean and Chinese, and has been recommended as a clinical indicator of insulin resistance [4, 5, 7, 16]. In experimental studies, insulin resistance was shown to promote the secretion of larger and TG over-enriched VLDL particles [17, 18], but decrease the concentration of HDL-C. Thus, insulin resistance contributes to the increase of TG/HDL-C. On the other hand, insulin resistance promotes NAFLD by inducing lipolysis of adipose tissue TG and de novo synthesis of TG in the liver [19, 20].…”

Section: Discussionmentioning

confidence: 99%

Triglycerides to high-density lipoprotein cholesterol ratio as a surrogate for nonalcoholic fatty liver disease: a cross-sectional study

et al. 2019

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BackgroundTriglycerides (TG) to high-density lipoprotein cholesterol (HDL-C) ratio (TG/HDL-C) has been recommended as a surrogate marker for insulin resistance. In the present study, we aimed to investigate the relationship between TG/HDL-C and NAFLD in an apparently healthy population.MethodsA total of 18,061 subjects who participated in a health checkup program were included. NAFLD was diagnosed by ultrasonography.ResultsThe prevalence rate of NAFLD was 24.8% in the whole population, and progressively increased across the quartiles of TG/HDL-C (4.9, 14.1, 26.8 and 53.5%, respectively, P < 0.001). After adjustment for confounding factors, TG/HDL-C was independently associated with the risk of NAFLD. Compared with the first quartile of TG/HDL-C (Q1), the odds ratios (95% confidence intervals) for NAFLD in the increasing quartiles (Q2-Q4) were 2.1(1.8–2.6), 3.6 (3.0–4.3) and 9.2(7.6–11.1), respectively. In addition, the area under receiver operator characteristic curve (95% confidence interval) of TG/HDL-C for NAFLD was 0.85 (0.84–0.86) in women and 0.79 (0.78–0.80) in men, significantly higher than that of TG, TC, LDL-C, HDL-C, ALT and AST (P < 0.05). The optimal cutoff point of TG/HDL-C for detection of NAFLD was 0.9 in women (sensitivity = 78.8%, specificity = 77.3%) and 1.4 in men (sensitivity = 70.7%, specificity = 73.5%).ConclusionsTG/HDL-C is independently associated with NAFLD in apparently healthy individuals and may be used as a surrogate for NAFLD.

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“…It causes the dysregulation of adipocytokines, such as adiponectin, PAI-1, IL-6, and MCP-1, leading to metabolic syndrome [134]. IR also activates SREBP-1c and inhibits acetyl-coenzyme A carboxylase, leading to reduced PPAR-a expression and the promotion of large-sized and TG-rich VLDL synthesis and secretion [135].…”

Section: Metabolic Syndromementioning

confidence: 99%

Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences

Hong

Choi

2020

IJMS

198

151

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The prevalence of sarcopenic obesity is increasing worldwide, particularly amongst aging populations. Insulin resistance is the core mechanism of sarcopenic obesity and is also associated with variable cardiometabolic diseases such as cardiovascular disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. Fat accumulation in muscle tissue promotes a proinflammatory cascade and oxidative stress, leading to mitochondrial dysfunction, impaired insulin signaling, and muscle atrophy. To compound the problem, decreased muscle mass aggravates insulin resistance. In addition, the crosstalk between myokines and adipokines leads to negative feedback, which in turn aggravates sarcopenic obesity and insulin resistance. In this review, we focus on the molecular mechanisms linking sarcopenic obesity and insulin resistance with various biological pathways. We also discuss the impact and mechanism of sarcopenic obesity and insulin resistance on cardiometabolic disease.

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Overproduction of altered VLDL in an insulin-resistance rat model: Influence of SREBP-1c and PPAR-α

Cited by 20 publications

References 30 publications

Attenuation of insulin resistance in rats by agmatine: role of SREBP-1c, mTOR and GLUT-2

Attenuation of insulin resistance in rats by agmatine: role of SREBP-1c, mTOR and GLUT-2

Triglycerides to high-density lipoprotein cholesterol ratio as a surrogate for nonalcoholic fatty liver disease: a cross-sectional study

Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences

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