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Effect of increased endogenous glucose levels within Type 2 diabetes on cellular lipid profiles / Rachel Churm, John Barry, Scott Caplin, Jeffrey Davies, Jeffrey Stephens, Sarah Prior
Endocrine Abstracts, Volume: 48, Issue: 2
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Background & Aims: ATP binding cassette subfamily G1 (ABCG1) is involved in mediating cholesterol efflux and modulating cellular lipid homeostasis. It is influenced by endogenous glucose and our aim was to examine the relationship between ABCG1 expression and lipid profiles within the increased...
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Background & Aims: ATP binding cassette subfamily G1 (ABCG1) is involved in mediating cholesterol efflux and modulating cellular lipid homeostasis. It is influenced by endogenous glucose and our aim was to examine the relationship between ABCG1 expression and lipid profiles within the increased glucose levels of subjects with Type 2 diabetes (ODM).Methods: RNA was extracted from visceral fat collected from subjects undergoing abdominal surgery (bariatric and routine non-acute, non-malignant conditions). 30 subjects were categorised as non-obese (NO, n=10), obese (O, n=10) or ODM (n=10). Samples were examined using Real-Time qPCR and 2−ΔΔCt data analysis in order to determine gene expression changes. Lipid profiles were measured using a colorimetric assay on the Randox Daytona Plus™.Results & Conclusions: All three subject groups were well matched with weight/BMI being the only significant differences between clinical parameters. There was no overall change in the expression of ABCG1 when comparing the O to the NO group. Reduced expression of ABCG1 was observed in ODM compared to O and the NO group (ABCG1=2.0-fold and 2.4- fold decrease, respectively). An increase in plasma glucose correlate with the reduced expression of ABCG1 (P<0.05). Data suggests that this is having a knock on effect on lipid profile markers. Within the ODM there is a significant decrease in plasma levels of total cholesterol, HDL and LDLs (P; <0.05, <0.05, <0.01 respectively). This decrease in plasma lipids is independent of prescribed statin use. Therefore, hypothesised to be the result of a reduction in cholesterol export from the cell and consequently cellular lipid retention.
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