Fasting hyperinsulinemia, hyperproinsulinemia, high FPI/SI ratio, and IR were defined by >95th percentile of our healthy reference population; that is, FSI > 11.
As listed in Table 2, although there was no significant decrease of HOMA-B in subjects before diagnosis of T2DM, the prevalence of IR and the disproportionate hyperproinsulinemia were increasingly verified in the group of NGT-FDRs (2-fold to 4-fold) and both were about 10-fold higher in newly diagnosed T2DM group compared to control group, whereas the prevalence of hyperinsulinemia was peaked to 27.
Two major hypotheses have been expounded to explain the hyperproinsulinemia
in type 2 diabetes: the increased release of proinsulin might result from an intrinsic defect in proinsulin processing, leading to an increased release of immature insulin precursors and thus contributing to the impairment in [beta]-cell function in type 2 DM.
segregates young adult patients with newly diagnosed autoimmune (type 1) and non-autoimmune (type 2) diabetes.
is a common feature of the insulin resistance (IR) syndrome.
Sagittal abdominal diameter is a strong anthropometric marker of insulin resistance and hyperproinsulinemia
in obese men.
and proinsulin-to-insulin ratios in Swedish middle-aged men: association with glycemia and insulin resistance but not with family history of diabetes.
In this study, total proinsulin concentrations were in accord with previously published reports of 10% (proinsulin:insulin) for samples from persons without diabetes and 20% for patients with type 2 diabetes (24), with no samples displaying inappropriate hyperproinsulinemia (25).
A novel point mutation in the insulin gene giving rise to hyperproinsulinemia.
Increased secretory demand rather than a defect in the proinsulin conversion mechanism causes hyperproinsulinemia
in a glucose-infusion rat model of non-insulin-dependent diabetes mellitus.
However, in patients suffering from type I (10) or type II diabetes (11-13), familial hyperproinsulinemia
(14,15), or insulinoma (16), the insulin concentration can be overestimated by the relatively high concentrations of proinsulin and conversion intermediates.
Proinsulin-like material is increased in clinical conditions such as insulinoma (6-9), familial hyperproinsulinemia
(10-13), and non-insulin-dependent diabetes mellitus (NIDDM) (3,9,14-17).