Research article summary (published 30 Jul 1999):

Correlation of acetylator phenotype with peripheral, autonomic and central neuropathy in Northern Indian non-insulin-dependent diabetes mellitus patients.

Full Abstract

OBJECTIVES: Genetic susceptibility to diabetic neuropathy has been suspected and tentatively explored; however, diabetic autonomic and central neuropathies are poorly investigated areas. Previous trials correlating types of diabetes and diabetic neuropathy with acetylator dimorphisms have not been conclusive. The present study was designed to test peripheral neuropathy, autonomic neuropathy and integrity of central conduction pathways in patients of non-insulin-dependent diabetes mellitus (NIDDM), and to correlate the findings with the acetylator phenotype. METHODS: Twenty-six patients of NIDDM with stable glycaemic control and 11 age- and sex-matched control subjects were recruited, clinically examined and investigated with glycaemic and lipid profile, renal function tests, nerve conduction studies (sensory and motor), auditory brain stem evoked responses (ABERs) and somatosensory evoked potentials (SEPs). Acetylator status of the subjects was determined by sulphadimidine test. RESULTS: Out of 26 NIDDM patients, eight (30.7%; group 1A) were slow acetylators and 18 (69.3%; group 1B) were fast acetylators. The distribution of slow and rapid acetylators in both the groups was similar. Glycaemic and lipid profiles and 24-h urinary albumin excretion in groups 1A and 1B were also similar. Motor nerve conduction velocity, latency of F wave, sensory nerve conduction and amplitudes of sensory nerve action potentials were not different between fast and slow acetylator NIDDM patients. On testing for ABERs, there were no statistically significant differences in peak latencies of waves I, III and V; interpeak latencies (IPLs) I-III, III-V and I-V; amplitude of waves I, III and V on both sides between NIDDM patients and controls. However, peak latencies of wave III (P < 0.01), wave V (P < 0.005), IPLs I-III and I-V (P < 0.005), IPLs III-V (P < 0.05), and amplitudes of wave I (P < 0.05) and wave V (P < 0.05) on the left side were significantly different in slow acetylator NIDDM patients. Increase on the right side for the same group was statistically significant for IPLs I-III and I-V (P < 0.05). SEPs showed no statistically significant difference between NIDDM patients and controls, and slow and fast acetylator NIDDM patients. CONCLUSIONS: No significant association of acetylator status with peripheral neuropathy in NIDDM subjects was observed in the present study. However, central neural conduction, primarily tested by ABERs, was significantly delayed in slow acetylators compared with fast acetylator NIDDM patients. Hence, there may be a predisposition to neuropathy in this group of patients, and such a predisposition may be better detected by studying central rather than peripheral nervous conduction pathways in NIDDM patients.

Author information

Author/s: Misra, A (A); Mittal, V (V); Jain, S (S); Bajaj, J S (JS);

Affiliation: Centre of Clinical Pharmacology, Department of Internal Medicine, All India Institute of Medical Sciences, New Delhi. anoopmisra(-atsign-)hotmail.com

Journal and publication information

Publication Type: Clinical Trial; Journal Article

Journal: European journal of clinical pharmacology (Eur J Clin Pharmacol), published in GERMANY. (Language: eng)

Reference: 1999-Aug; vol 55 (issue 6) : pp 419-24

Dates: Created 1999/10/12; Completed 1999/10/12; Revised 2004/11/17;

PMID: 10492053, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

External Links for this article
(including full text providers, if available):

Click Electronic Full-text Provider Links to see options for finding the electronic full text links to this article. Note there may be a subscription or fee required for access to the full text. See our FAQ for information on finding FREE full text articles.

This article may also be located in paper journal collections available in many libraries. Use the Journal and Publication Information above to find the full article.

MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Adult Arylamine N-Acetyltransferase - genetics; metabolism Autonomic Nervous System Diseases - complications; physiopathology Central Nervous System Diseases - complications; physiopathology Diabetes Mellitus, Type 2 - enzymology; ethnology; physiopathology Diabetic Neuropathies - enzymology; metabolism; physiopathology Evoked Potentials, Auditory Evoked Potentials, Somatosensory Humans

Humans India Kidney Function Tests Middle Aged Motor Neurons - physiology Neural Conduction Neurons, Afferent - physiology Peripheral Nervous System Diseases - complications; physiopathology Phenotype

Associated Chemicals: Arylamine N-Acetyltransferase (EC 2.3.1.5)

Related articles

These are the highest related articles currently in the database:

• Molecular genotyping of N-acetylation polymorphism to predict phenotype. 30 Aug 1992
• Demonstration of slow acetylator genotype of N-acetyltransferase in isoniazid neuropathy using an archival hematoxylin and eosin section of a sural nerve biopsy specimen. 30 Dec 1995
• Determination of CYP1A2 and NAT2 phenotypes in human populations by analysis of caffeine urinary metabolites. 30 May 1992
• N-acetyltransferase polymorphism. Comparison of phenotype and genotype in humans. 6 Aug 1991
• A simplified and rapid test for acetylator phenotyping by use of the peak height ratio of two urinary caffeine metabolites. 29 Apr 1989
• N-acetyltransferase activity--a susceptibility factor in human bladder carcinogenesis. 27 Feb 1995
• Dapsone acetylation by human liver arylamine N-acetyltransferases and interaction with antiopportunistic infection drugs. 30 Mar 1995
• Analysis of within-subject variation of caffeine metabolism when used to determine cytochrome P4501A2 and N-acetyltransferase-2 activities. 27 Feb 1995
• Slow N-acetylation genotype is a susceptibility factor in occupational and smoking related bladder cancer. 30 Jan 1995

See 100+ related articles.

Related Article Map

Legend: - FREE Full text Article. - Abstract only. - Title only. More help.

See a large map of 100+ related articles.