Quadriceps (Q) and gastrocnemius (G) muscle capillary basement membrane width (CBMW) were measured in 18 pairs of monozygotic (MZ) twins. Thirteen of these twin pairs were discordant for insulin-dependent diabetes (IDD) and five pairs were concordant for either IDD (two pairs) or for non-insulin-dependent diabetes (NIDD). In 12 of the 13 nondiabetic (ND) twin mates of IDD, 50 oral glucose tolerance tests performed in the years before or after determination of CBMW revealed mean blood glucose levels in the 36–52 percentile range, compared with normal controls.
The mean (±SD) age at the onset of IDD in discordant twins was 18.7 ± 10.1 (range 8–37) yr and the mean duration of discordance at the time of biopsy was 13.6 ± 8.3 (range 3–32) yr. CBMW data were compared within each twin (Q versus G) and between twin mates and age- and sex-matched controls. Overall, CBMW of IDD twins was greater than that of their ND twin mates. Differences between IDD and ND twins, however, were much more marked in gastrocnemius (1859 ± 643 versus 1222 ± 307 Å, P < 0.0003) than in quadriceps (1291 ±319 versus 1112 ± 302 Å; P < 0.04). CBMW in gastrocnemius was significantly thicker than that in the quadriceps of IDD twins (t = 4.55, P < 0.0008) but not in their ND twin mates (t = 1.15, P < 0.27). CMBW was significantly thicker in IDD than in their ND twin mates (in quadriceps and/or gastrocnemius) in 10 of the 12 twin pairs. Ten of 12 IDD twins (no tissue was available from 1 IDD twin) and 8 of their 13 ND twin mates had evidence of quad-riceps CBMT compared with controls. Repeat biopsies (taken 3–4 yr after the initial biopsy) of quadriceps muscle from five pairs of MZ twins (discordant for IDD) revealed only minor changes in mean CBMW in all but 1 subject.
The muscle CBMW of IDD twins is frequently, but not invariably, “thicker” than that of their ND twin mates. Although some ND twin mates of IDD may have “thick” CBM, this observation does not necessarily imply a greater propensity to development of diabetes.
Further studies are required to elucidate the interactions of genetic and local tissue-environmental factors in modulating the development of diabetic vascular disease.