Dyslipidemia-Induced Neuropathy in Mice
Open accessAbstract
OBJECTIVE: Neuropathy is a frequent and severe complication of diabetes. Multiple metabolic defects in type 2 diabetic patients result in oxidative injury of dorsal root ganglia (DRG) neurons. Our previous work focused on hyperglycemia clearly demonstrates induction of mitochondrial oxidative stress and acute injury in DRG neurons; however, this mechanism is not the only factor that produces neuropathy in vivo. Dyslipidemia also correlates with the development of neuropathy, even in pre-diabetic patients. This study was designed to explore the contribution of dyslipidemia in neuropathy. RESEARCH DESIGN AND METHODS: Mice (n = 10) were fed a control (10% kcal %fat) or high-fat (45% kcal %fat) diet to explore the impact of plasma lipids on the development of neuropathy. We also examined oxidized lipid–mediated injury in cultured DRG neurons from adult rat using oxidized LDLs (oxLDLs). RESULTS: Mice on a high-fat diet have increased oxLDLs and systemic and nerve oxidative stress. They develop nerve conduction velocity (NCV) and sensory deficits prior to impaired glucose tolerance. In vitro, oxLDLs lead to severe DRG neuron oxidative stress via interaction with the receptor lectin-like oxLDL receptor (LOX)-1 and subsequent NAD(P)H oxidase activity. Oxidative stress resulting from oxLDLs and high glucose is additive. CONCLUSIONS: Multiple metabolic defects in type 2 diabetes directly injure DRG neurons through different mechanisms that all result in oxidative stress. Dyslipidemia leads to high levels of oxLDLs that may injure DRG neurons via LOX-1 and contribute to the development of diabetic neuropathy.
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Low-density lipoproteins (LDL) can undergo oxidation and glycation processes, amplifying the oxidative stress already triggered by excess glucose.
“Low-density lipoproteins (LDL) can undergo oxidation and glycation processes, amplifying the oxidative stress already triggered by excess glucose [38].”
From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [38]
The Results section reports that oxidized LDL increased mitochondrial superoxide in cultured DRG neurons, additively with high glucose; the Discussion also states that LDLs were oxidized. The passages do not establish that LDL undergoes glycation or that glycated LDL amplifies glucose-induced oxidative stress. Page numbers were not available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAlterations in lipid metabolism play a central role in the pathogenesis of diabetic autonomic neuropathy.
“In addition to hyperglycemia, alterations in lipid metabolism also play a central role in the pathogenesis of DAN.”
From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [38]
The Conclusions say dyslipidemia may contribute to diabetic neuropathy, and the Discussion reports lipid-related injury to dorsal root ganglion neurons. The paper examines sensory and peripheral neuropathy, not diabetic autonomic neuropathy, and does not establish that altered lipid metabolism plays a central role in its pathogenesis. (LLM, conf=0.88)
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- Authors
- Vincent, A. M., Hayes, J. M., McLean, L. L., Vivekanandan-Giri, A., Pennathur, S., & Feldman, E. L.
- Affiliations
- University of Michigan (US)
- Department of Medicine, University of Michigan, Ann Arbor, Michigan.
- Corresponding author
- Vincent, Andrea M.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2009-07-10
- Volume
- 58
- Issue
- 10
- Pages
- 2376-2385
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC2750230
- OpenAlex
- W2155399617
- Cited by
- 264
- References
- 51
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 20 · 2023: 15 · 2022: 15 · 2021: 23 · 2020: 19 · 2019: 14 · 2018: 11 · 2017: 12 · 2016: 9 · 2015: 9 · 2014: 31 · 2013: 14 · 2012: 21
- FWCI
- 10.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- University of Washington
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (U01DK076160, R24DK082841)
- Topics
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Health Sciences › Medicine › Neurology › Peripheral Neuropathies and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Aldose Reductase and Taurine
- Keywords
- dyslipidemia, diabetic neuropathy, dorsal root ganglion neurons, oxidized LDL, LOX-1, NADPH oxidase, oxidative stress, high-fat diet, nerve conduction velocity, sensory impairment, type 2 diabetes, hyperglycemia, plasma lipids
- MeSH terms
- Animals, Blood Glucose, Diabetes Mellitus, Type 2, Diabetic Neuropathies, Dietary Fats, Female, Ganglia, Spinal, Glucose Tolerance Test, Hindlimb, Insulin, Lipids, Lipoproteins, LDL, Mice, Inbred C57BL, Nerve Fibers, Neural Conduction, Neurons, Rats, Sprague-Dawley, Reactive Oxygen Species, Dyslipidemias, Scavenger Receptors, Class E, Mice, Rats, DNA Fragmentation
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