Premium Impaired maximum microvascular hyperaemia in patients with MODY 3 (hepatocyte nuclear factor‐1α gene mutations)Premium
Author(s)
Lee B. C.,
Appleton M.,
Shore A. C.,
Tooke J. E.,
Hattersley A. T.
Publication year1999
Publication title
diabetic medicine
Resource typeJournals
Summary Aims Functional abnormalities of blood flow and capillary pressure may be involved in the pathogenesis of diabetic microangiopathy. Important differences in microvascular behaviour are observed between Type 1 and Type 2 diabetes mellitus, raising the possibility that the pathogenesis of microangiopathy may differ between these. MODY3 patients have hyperglycaemia as a result of genetic defect of beta‐cell function rather than increased insulin resistance and are susceptible to microvascular complications and offer an opportunity to examine microvascular behaviour in this setting. Methods The maximum microvascular hyperaemic response to local heating of the skin was studied in 12 MODY3 patients and age and sex‐matched control subjects using laser Doppler fluximetry. Results Maximum hyperaemia was reduced in MODY3 patients (median 1.17 (range 0.88–1.92) V vs. 1.70 (1.07–2.19) V normal control subjects; P = 0.03) and thus was negatively associated with duration of diabetes ( r s = – 0.79; P = 0.002). Conclusions The results suggest that the duration of diabetes is a determinant of impaired microvascular hyperaemia in MODY3 patients. The pattern of vasodilatory impairment is similar to that observed in Type 1 diabetes mellitus and differs from that seen in Type 2 diabetes. This provides support for the concept that beta cell dysfunction and insulin resistance may have differing effects on microvascular behaviour.
Subject(s)blood flow , cardiology , diabetes mellitus , endocrinology , endothelial dysfunction , hyperaemia , insulin resistance , medicine , microangiopathy , pathogenesis , type 1 diabetes
Language(s)English
SCImago Journal Rank1.474
H-Index145
eISSN1464-5491
pISSN0742-3071
DOI10.1046/j.1464-5491.1999.00129.x
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