1. Recent molecular genetic studies have implicated the low-density-lipoprotein receptor gene locus (LDLR, at chromosome 19p13.2) in obesity in essential hypertensive patients and in the atherogenic lipoprotein phenotype. The present study examined genotypes for the obesity-associated ApaLI restriction fragment length polymorphism of LDLR, and genotypes for a hypertension-associated RsaI restriction fragment length polymorphism at the insulin receptor gene (INSR) locus, which is linked to LDLR, in relation to plasma lipids, body mass index and blood pressure in 27 obese and 57 non-obese Caucasians with severe essential hypertension, selected on the basis of having parents who were both hypertensive, and in 25 obese and 45 non-obese normotensive subjects selected on the basis of having parents who were both normotensive after the age of 50 years.

2. Plasma triacylglycerol and low-density-lipoprotein-cholesterol were elevated in hypertensive patients, but did not differ between the obese and non-obese hypertensive groups. Significant positive correlations were seen between body mass index and triacylglycerol and low-density-lipoprotein-cholesterol in the obese and non-obese hypertensive patients, respectively. In addition, obese hypertensive patients had significantly higher diastolic blood pressure than non-obese hypertensive patients.

3. The eight obese hypertensive patients who were homozygous for the obesity-associated 6.6 kb allele of the ApaLI restriction fragment length polymorphism of LDLR (‘6.6.kb homozygotes’) had a significantly higher body mass index [34 ± 6.0 (SD) kg/m2] than the 18 heterozygotes (29 ± 2.7 kg/m2) and the single subject who was homozygous for the 9.4 kb allele (29 kg/m2) (P = 0.012 by one-way analysis of variance). The body mass index of the eight hypertensive 6.6 kb homozygotes was also greater than the body mass index of 29 ± 2.4 kg/m2 observed for the eight obese normotensive 6.6 kb homozygotes. In addition, the eight obese hypertensive 6.6 kb homozygotes had a higher plasma triacylglycerol [4.2 ± 0.77 (SEM) mmol/l] than the 18 obese hypertensive heterozygotes (2.4 ± 0.33 mmol/l; P = 0.045). Non-obese hypertensive patients showed no significant gentotypic differences in relation to the LDLR restriction fragment length polymorphism.

4. In the normotensive group, however, the frequency of the 6.6 kb allele of the LDLR ApaLI restriction fragment length polymorphism in obese subjects (0.54) was not significantly greater than in non-obese subjects (0.48) [cf. the significantly (P = 0.004) different values of 0.63 and 0.39, respectively, in obese and non-obese hypertensive patients]. Moreover, the LDLR genotype showed no significant relationship to the body mass index or plasma lipids in the obese and non-obese normotensive groups.

5. In the case of genotypes for the INSR restriction fragment length polymorphism, the only difference was slightly higher total and low-density-lipoprotein-cholesterol in non-obese hypertensive patients who possessed the hypertension-associated 7.0 kb allele.

6. Comparison of combined genotypes for LDLR and INSR restriction fragment length polymorphisms in hypertensive patients indicated that each associated independently in the various groups.

7. In conclusion, the present study has found that in obese hypertensive patients a LDLR variant is associated with higher body mass index and plasma triacylglycerol, although a causal relationship of LDLR in obesity and hyperlipidaemia in such patients remains to be established.

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