Volume 28, Issue 6 pp. 2074-2082
ORIGINAL ARTICLE

Impact of the metabolic syndrome on peripheral nerve structure and function in type 2 diabetes

Tushar Issar

Tushar Issar

Prince of Wales Clinical School, UNSW Sydney, Sydney, NSW, Australia

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Shyam S. Tummanapalli

Shyam S. Tummanapalli

School of Optometry & Vision Science, UNSW Sydney, Sydney, NSW, Australia

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Adeniyi A. Borire

Adeniyi A. Borire

Prince of Wales Clinical School, UNSW Sydney, Sydney, NSW, Australia

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Natalie C. G. Kwai

Natalie C. G. Kwai

Prince of Wales Clinical School, UNSW Sydney, Sydney, NSW, Australia

Department of Exercise Physiology, UNSW Sydney, Sydney, NSW, Australia

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Ann M. Poynten

Ann M. Poynten

Department of Endocrinology, Prince of Wales Hospital, Sydney, NSW, Australia

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Ria Arnold

Ria Arnold

Department of Exercise Physiology, UNSW Sydney, Sydney, NSW, Australia

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Maria Markoulli

Maria Markoulli

School of Optometry & Vision Science, UNSW Sydney, Sydney, NSW, Australia

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Arun V. Krishnan

Corresponding Author

Arun V. Krishnan

Prince of Wales Clinical School, UNSW Sydney, Sydney, NSW, Australia

Correspondence

Arun V. Krishnan, Institute of Neurological Sciences, Prince of Wales Hospital, Randwick, NSW 2031, Australia.

Email: [email protected]

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First published: 07 March 2021
Citations: 16

Abstract

Background and purpose

There is a strong association between the metabolic syndrome in diabetes and the development of peripheral neuropathy; however, the pathophysiological mechanisms remain unknown.

Methods

Participants with type 2 diabetes and metabolic syndrome (T2DM/MetS, n = 89) and type 2 diabetes alone (T2DM; n = 59) underwent median nerve ultrasound and excitability studies to assess peripheral nerve structure and function. A subset of T2DM/MetS (n = 24) and T2DM (n = 22) participants underwent confocal microscopy to assess central and inferior whorl corneal nerve structure. Neuropathy severity was assessed using the modified Toronto Clinical Neuropathy Score (mTCNS). Diabetes groups were similar for age, sex distribution, diabetes duration, hemoglobin A1c, insulin treatment, and renal function. Sixty healthy controls similar for age and sex distribution were recruited for comparison.

Results

Participants with T2DM/MetS manifested with a greater mTCNS compared to T2DM (p < 0.05). Median nerve cross-sectional area was larger in the T2DM/MetS group compared to the T2DM cohort (p < 0.05). Participants with T2DM/MetS had reductions in central (all p < 0.01) and inferior whorl (all p < 0.05) nerve measures. Compared to T2DM, the T2DM/MetS group demonstrated more severe changes in nerve excitability measures, which was due to reduced sodium channel permeability and sodium–potassium pump function. In comparison, only sodium channel permeability was reduced in the T2DM group.

Conclusions

Compared to participants with type 2 diabetes alone, those with diabetes and metabolic syndrome manifested greater alterations in peripheral nerve structure and function, which may be due to reduced function of the sodium–potassium pump.

CONFLICT OF INTERESTS

None.

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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