Hyperlipidemia Influences the Accuracy of Glucometer-Measured Blood Glucose Concentrations in Genetically Diverse Mice

Shi, Lisa J.; Tang, Xiwei; He, Jiang; Shi, Weibin

doi:10.1016/j.amjms.2021.06.014

Cited by 7 publications

(12 citation statements)

References 20 publications

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“…Plasma glucose levels were measured with a Sigma assay kit (Cat. # GAHK20, Saint Louis, MO, USA), an assay based on the hexokinase oxidase reaction, as we reported [ 25 ]. In brief, 6 μL of diluted plasma samples (3× in water), together with standards and controls, were loaded in a 96-well plate and mixed with 150 µL of assay reagent per well.…”

Section: Methodsmentioning

confidence: 99%

Genetic Connection between Hyperglycemia and Carotid Atherosclerosis in Hyperlipidemic Mice

Shi

Chagari

et al. 2022

Genes

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Type 2 diabetes (T2D) is a major risk for atherosclerosis and its complications. Apoe-null (Apoe−/−) mouse strains exhibit a wide range of variations in susceptibility to T2D and carotid atherosclerosis, with the latter being a major cause of ischemic stroke. To identify genetic connections between T2D and carotid atherosclerosis, 145 male F2 mice were generated from LP/J and BALB/cJ Apoe−/− mice and fed 12 weeks of a Western diet. Atherosclerotic lesions in the carotid arteries, fasting, and non-fasting plasma glucose levels were measured, and genotyping was performed using miniMUGA arrays. Two significant QTL (quantitative trait loci) on chromosomes (Chr) 6 and 15 were identified for carotid lesions. The Chr15 QTL coincided precisely with QTL Bglu19 for fasting and non-fasting glucose levels. Carotid lesion sizes showed a trend toward correlation with fasting and non-fasting glucose levels in F2 mice. The Chr15 QTL for carotid lesions was suppressed after excluding the influence from fasting or non-fasting glucose. Likely candidate genes for the causal association were Tnfrsf11b, Deptor, and Gsdmc2. These results demonstrate a causative role for hyperglycemia in the development of carotid atherosclerosis in hyperlipidemic mice.

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Section: Methodsmentioning

confidence: 99%

Genetic Connection between Hyperglycemia and Carotid Atherosclerosis in Hyperlipidemic Mice

Shi

Chagari

et al. 2022

Genes

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“…Fasting blood was collected after 12 weeks of the Western diet. All blood samples were drawn from the retro-orbital veins with the animals being anesthetized by isoflurane inhalation and prepared as reported [ 25 ]. All procedures were performed in accordance with the National Institutes of Health guidelines and approved on 20 January 2022 by the Institutional Animal Care and Use Committee (protocol #: 3109).…”

Section: Methodsmentioning

confidence: 99%

“…Plasma glucose concentrations were measured using a Sigma assay kit (Cat. # GAHK20, Saint Louis, MO, USA) as reported [ 25 ]. The plasma samples collected from the Western diet-fed mice were diluted 3× in H 2 O, and those from the chow diet-fed mice were not diluted.…”

Section: Methodsmentioning

confidence: 99%

“…The plasma concentrations of total and HDL cholesterol and triglycerides were measured using reagents from Stanbio Labs (Boeme, TX, USA) and HDL precipitating reagent from Wako Diagnostics (Mountain View, CA, USA) as reported [ 25 ]. For the assay of total cholesterol concentrations in the Western diet-fed mice, plasma samples were diluted 3× with H 2 O. Non-HDL cholesterol was calculated as the difference between the total and HDL cholesterol levels.…”

Section: Methodsmentioning

confidence: 99%

“…Many studies, including prospective ones, have shown that low levels of HDL cholesterol and elevated non-HDL cholesterol and triglyceride levels are associated with increased risk of developing T2D [ 20 , 21 , 22 ]. Similarly, plasma non-HDL and triglyceride levels show positive correlations with glucose levels in segregating an F2 population derived from Apoe -/- mouse strains [ 23 , 24 , 25 ]. However, several lines of evidence have suggested a protective role for circulating lipids in T2D.…”

Section: Introductionmentioning

confidence: 99%

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Genetic Evidence for a Causal Relationship between Hyperlipidemia and Type 2 Diabetes in Mice

Shi

Tang

et al. 2022

IJMS

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Dyslipidemia is considered a risk factor for type 2 diabetes (T2D), yet studies with statins and candidate genes suggest that circulating lipids may protect against T2D development. Apoe-null (Apoe-/-) mouse strains develop spontaneous dyslipidemia and exhibit a wide variation in susceptibility to diet-induced T2D. We thus used Apoe-/- mice to elucidate phenotypic and genetic relationships of circulating lipids with T2D. A male F2 cohort was generated from an intercross between LP/J and BALB/cJ Apoe-/- mice and fed 12 weeks of a Western diet. Fasting, non-fasting plasma glucose, and lipid levels were measured and genotyping was performed using miniMUGA arrays. We uncovered a major QTL near 60 Mb on chromosome 15, Nhdlq18, which affected non-HDL cholesterol and triglyceride levels under both fasting and non-fasting states. This QTL was coincident with Bglu20, a QTL that modulates fasting and non-fasting glucose levels. The plasma levels of non-HDL cholesterol and triglycerides were closely correlated with the plasma glucose levels in F2 mice. Bglu20 disappeared after adjustment for non-HDL cholesterol or triglycerides. These results demonstrate a causative role for dyslipidemia in T2D development in mice.

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Identification of Mep1a as a susceptibility gene for atherosclerosis in mice

Grainger

Pilar

et al. 2021

Genetics

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Atherosclerosis is the underlying cause of heart attack, ischemic stroke and peripheral arterial disease, and genetic factors involved remain mostly unidentified. We previously identified a significant locus on mouse chromosome 17 for atherosclerosis, Ath49, in an intercross between BALB/c and SM strains. Ath49 partially overlaps in the confidence interval with Ath22 mapped in an AKR x DBA/2 intercross. Bioinformatics analysis prioritized Mep1a, encoding meprin 1α metalloendopeptidase, as a likely candidate gene for Ath49. To prove causality, Mep1a-/-Apoe-/- mice were generated and compared with Mep1a+/+Apoe-/- mice for atherosclerosis development. Mep1a was found abundantly expressed in atherosclerotic lesions but not in healthy aorta and liver of mice. Mep1a -/- Apoe-/- mice exhibited significant reductions in both early and advanced lesion sizes. Loss of Mep1a led to decreased necrosis but increased macrophage and neutrophil contents in advanced lesions, reduced plasma levels of CXCL5 and an oxidative stress biomarker. In addition, Mep1a-/- mice had a significantly reduced triglyceride levels on a chow diet. Thus, Mep1a is a susceptibility gene for atherosclerosis and aggravates atherosclerosis partially through action on oxidative stress and inflammation.

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Hyperlipidemia Influences the Accuracy of Glucometer-Measured Blood Glucose Concentrations in Genetically Diverse Mice

Cited by 7 publications

References 20 publications

Genetic Connection between Hyperglycemia and Carotid Atherosclerosis in Hyperlipidemic Mice

Genetic Connection between Hyperglycemia and Carotid Atherosclerosis in Hyperlipidemic Mice

Genetic Evidence for a Causal Relationship between Hyperlipidemia and Type 2 Diabetes in Mice

Identification of Mep1a as a susceptibility gene for atherosclerosis in mice

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