S. Jacob et al., IS MILD HYPERTRIGLYCERIDEMIA ONE TIP OF T HE ICEBERG OF INSULIN-RESISTANCE, Nieren- und Hochdruckkrankheiten, 22(7), 1993, pp. 335-338
Cardiovascular patients often present with several risk factors; the c
lustering of hyperlipemia, hypertension, obesity and glucose intoleran
ce is called the >>metabolic syndrome<< and resistance to insulin stim
ulated glucose uptake is thought to play a major role. Therefore, in a
hypertensive patient, hyperlipemia could point at the presence of thi
s syndrome; most often, however, moderate hypertriglyceridemia (hTG) i
s not considered to be a risk factor, especially as some intervention
studies did not define TG as an indipendent risk factor. In the presen
t investigation, we looked at the risk profile of hypertensive patient
s with mildly elevated TG (150-230 mg%) and a normal glucose loading t
est; venous insulin levels were determined during the test (Enzyme Imm
uno-Assay, Boehringer Mannheim, Germany). Twenty seven patients were c
ompared with seventeen healthy volunteers. The risk patients, although
showing lipids and glucose tolerance within the normal range, had a s
ignificantly increased atherogenic risk profile, when compared to the
controls, with raised levels of total-cholesterol (237 vs 202 mmg%,
= p less-than-or-equal-to 0.05), LDL-C (125 vs 147 mg%), triglyceride
s (179 vs 111 mg%) and lower HDL-C (43 vs 58 mg%*). Plasma glucose wa
s significantly higher at all intervals (0-60-120 min) and insulin lev
els were almost doubled at 60 (116 vs 60 uU/ml) and 120 minutes (92 v
s 36 uU/ml). The latter finding reveals a drastic decrease in periphe
ral insulin-stimulated glucose uptake in the risk group, most probably
caused by insulinresistance. Due to the >>normal<< laboratory values,
these patients would not have been considered to be at increased card
iovascular risk. The additional determination of insulin during an ora
l glucose load was able to unmask the impaired insulin sensitivity. Th
us, in the hypertensive patient the dangerous Metabolic Syndrome is de
tectable via the marginally elevated triglycerides.