ArticleThe Journal of physiology2009
Myocardial metabolism of triacylglycerol-rich lipoproteins in type 2 diabetes.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Changes in the Metabolome of Different Tissues in Response to Streptozotocin Diabetes and Mildronate Exposure: A Metabolomic Assessment.Metabolites · 2026Article
- Radiolabeling lipoproteins to study and manage disease.European journal of nuclear medicine and molecular imaging · 2025Review
- Very low-density lipoprotein receptor mediates triglyceride-rich lipoprotein-induced oxidative stress and insulin resistance.American journal of physiology. Heart and circulatory physiology · 2024Article
- Obesity and lipid metabolism in the development of osteoporosis (Review).International journal of molecular medicine · 2024Review
- Mitochondrial dysfunction and its impact on diabetic heart.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Leptin- and leptin receptor-deficient rodent models: relevance for human type 2 diabetes.Current diabetes reviews · 2014Review
- Antioxidant treatment improves neonatal survival and prevents impaired cardiac function at adulthood following neonatal glucocorticoid therapy.The Journal of physiology · 2013Article
- Direct evidence of progressive cardiac dysfunction in a transgenic mouse model of Huntington's disease.Journal of Huntington's disease · 2012Article
- Very-low-density lipoprotein: complex particles in cardiac energy metabolism.Journal of lipids · 2011Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac utilisation of very-low-density lipoprotein (VLDL) and chylomicrons (CM) was investigated in the ZDF rat model of type 2 diabetes, in order to define the role of triacylglycerol (TAG) metabolism in the development of contractile dysfunction. Hearts from obese diabetic and lean littermate control rats were perfused with VLDL and CM from diabetic and control rats. Metabolic fate of the lipoprotein TAG and contractile function were examined. Myocardial utilisation of both VLDL- and CM-TAG was increased in the diabetic state. Diabetic hearts oxidised diabetic lipoprotein-TAG to a greater extent than control lipoproteins; glucose oxidation was decreased. There was no difference in lipoprotein-TAG assimilation into diabetic heart lipids; diabetic lipoproteins were, however, a poor substrate for control heart tissue lipid accumulation. Although the proportion of exogenous lipid incorporated into tissue TAG was increased in diabetic hearts perfused with control lipoproteins, this effect was not seen in diabetic hearts perfused with diabetic lipoproteins. Myocardial heparin-releasable lipoprotein lipase (LPL) activity was moderately increased in the diabetic state, and diabetic lipoproteins increased tissue-residual LPL activity. Cardiac hydraulic work was decreased only in diabetic hearts perfused with diabetic CM. Compositional analysis of diabetic variant lipoproteins indicated changes in size and apoprotein content. Alterations in cardiac TAG-rich lipoprotein metabolism in type 2 diabetes are due to changes in both the diabetic myocardium and the diabetic lipoprotein particle; decreased contractile function is not related to cardiac lipid accumulation from TAG-rich lipoproteins but may be associated with changes in TAG-fatty acid oxidation.
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