Journal
DIABETOLOGIA
Volume 62, Issue 9, Pages 1539-1549Publisher
SPRINGER
DOI: 10.1007/s00125-019-4959-1
Keywords
Diabetes; Diabetic complications; Lipid metabolism; Omics; Review; Specific mechanisms
Categories
Funding
- National Institutes of Health [1R24082841, P30DK081943, R01EY020582, R01EY029349, R01EY020823, R01EY020895, P30EY007003]
- Kellogg Eye Center Core Center for Vision Research [P30DK081943, R24DK08284, P30DK89503]
- Novo Nordisk Foundation [NNF14OC0011633]
- Milstein, Nathan and Rose Research Fund
- Program for Neurology Research Discovery
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Diabetes adversely affects multiple organs, including the kidney, eye and nerve, leading to diabetic kidney disease, diabetic retinopathy and diabetic neuropathy, respectively. In both type 1 and type 2 diabetes, tissue damage is organ specific and is secondary to a combination of multiple metabolic insults. Hyperglycaemia, dyslipidaemia and hypertension combine with the duration and type of diabetes to define the distinct pathophysiology underlying diabetic kidney disease, diabetic retinopathy and diabetic neuropathy. Only recently have the commonalities and differences in the metabolic basis of these tissue-specific complications, particularly those involving local and systemic lipids, been systematically examined. This review focuses on recent progress made using preclinical models and human-based approaches towards understanding how bioenergetics and metabolomic profiles contribute to diabetic kidney disease, diabetic retinopathy and diabetic neuropathy. This new understanding of the biology of complication-prone tissues highlights the need for organ-specific interventions in the treatment of diabetic complications.
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