Hyperproinsulinemia

05/01/1997 - "A novel point mutation in the insulin gene giving rise to hyperproinsulinemia."
08/01/1994 - "Hyperproinsulinemia and insulin deficiency in the diabetic Psammomys obesus."
05/01/1992 - "We examined whether this technique could detect five mutations that had previously been identified in the insulin genes of patients with abnormal insulin or familial hyperproinsulinemia. "
07/01/1990 - "Interestingly, the same His65 mutation has been identified in the insulin gene of a Japanese kindred with familial hyperproinsulinemia. "
12/01/1988 - "A coding mutation in the human insulin gene (His-B10----Asp) is associated with familial hyperproinsulinemia. "

07/22/2011 - "The findings demonstrate that the perturbation of PIHO results in defects in the subsequent conversion process of proinsulin and is a contributor to the occurrence of disproportionate hyperproinsulinemia in diabetes."
09/01/2003 - "These findings provide evidence that the elevation of plasma proinsulin levels found in patients with familial hyperproinsulinemia is caused by the disruption of CPE-mediated sorting of mutant proinsulins to the regulated secretory pathway."
09/01/2003 - "In familial hyperproinsulinemia, specific mutations in the proinsulin gene are linked with a profound increase in circulating plasma proinsulin levels. "
09/01/2003 - "Disruption of a receptor-mediated mechanism for intracellular sorting of proinsulin in familial hyperproinsulinemia."
04/01/1996 - "In conclusion, our data demonstrate hyperproinsulinemia in a three-generation Caucasian family due to heterozygous mutant Arg65-->His proinsulin. "

08/01/1995 - "To address the question of whether genetic factors contribute to hyperproinsulinemia, we measured fasting levels of PI immunoreactivity, intact INS, and C peptide (CP) in 12 pairs of monozygotic twins discordant for NIDDM for a mean (+/- SEM) period of 9 +/- 3 yr. Thirteen age- and body mass index-matched healthy subjects without any family history of NIDDM acted as controls. "
11/01/2005 - "GDM is not independently associated with hyperproinsulinemia as measured by the proinsulin-to-C-peptide ratio. "
06/01/1979 - "A structural abnormality appears to underlie familial hyperproinsulinemia proinsulin, which impairs its cleavage at the B-chain-C-peptide linkage site."
06/01/1979 - "These data indicate that familial hyperproinsulinemia proinsulin is normally cleaved at the C-peptide-A-chain linkage site. "
10/01/1997 - "The diabetic subjects on diet therapy had relative hyperproinsulinemia, assessed relative to C-peptide concentrations, fasting and in response to hyperglycemic clamping and arginine, compared with control subjects. "

01/01/2020 - "The reduced plasma levels of acylated ghrelin in patients were significantly correlated with obesity, hyperinsulinemia, and hyperproinsulinemia (P = 0.029 and P = 0.028, respectively). "
01/01/2020 - "To study if plasma levels of ghrelin is associated with obesity and hyperinsulinemia or hyperproinsulinemia in patients with insulinoma, and to detect the expression of ghrelin and its receptor in insulinoma. "

06/01/1979 - "Our studies show that trypsin converts familial hyperproinsulinemia proinsulin to insulin more slowly than it converts a 131I-labeled porcine proinsulin marker. "

06/01/1979 - "Studies with two human C-peptide antisera that differ in their relative immunoreactivity with human C-peptide and proinsulin showed that the two antisera reacted equally with familial hyperproinsulinemia proinsulin, suggesting that it is a partially cleaved proinsulin intermediate. "

08/06/2002 - "There is marked hyperproinsulinemia but without impairment of glucose tolerance. "
04/01/1999 - "These data add direct support to the view that a disproportionate hyperproinsulinemia can result from a sustained activation of human beta-cells after prolonged exposure to elevated glucose levels."
10/01/1987 - "In conclusion, chronic endogenous hyperinsulinemia (and hyperproinsulinemia) in humans is associated with a defect in peripheral glucose utilization that is only partially resolved 2 years after tumor removal."
01/01/2006 - "However, the adolescent diabetic subjects retained a first-phase insulin response to glucose that was comparable to lean controls and did not have hyperproinsulinemia or hyperglucagonemia."
08/01/2000 - "Hyperproinsulinemia is not a characteristic finding in glucose-tolerant offspring of type II diabetic probands with deficient insulin secretion or insulin-resistant phenotype. "

06/01/2008 - "To explore the association between 801C>T and 847C>T polymorphisms of the human carboxypeptidase E (CPE) gene exon5, which could cause hyperproinsulinemia, and the angiographical characteristics of coronary atherosclerosis. "
01/01/2019 - "eIF4G1 and carboxypeptidase E axis dysregulation in O-GlcNAc transferase-deficient pancreatic β-cells contributes to hyperproinsulinemia in mice."
07/01/2011 - "Defects in insulin processing enzymes including prohormone convertases 1/3 and 2, and carboxypeptidase E (CPE) can lead to β-cell stress and hyperproinsulinemia, both of which are features of type 2 diabetes. "
11/02/2023 - "Proinsulin processing includes removal of several C-terminal basic amino acids and is performed principally by the exopeptidase carboxypeptidase E (CPE), and mutations in CPE or other prohormone convertase enzymes (PC1/3 and PC2) result in hyperproinsulinemia. "

08/01/1989 - "These data strongly suggest that this family is a new case of familial hyperproinsulinemia, and the defect resides in the proinsulin molecule, not in the converting enzymes."
03/01/1995 - "Thus, hyperproinsulinemia induced by chronic hyperglycemia likely results from increased beta cell secretory demand, rather than a defect in the proinsulin processing enzymes per se."
07/01/2011 - "Defects in insulin processing enzymes including prohormone convertases 1/3 and 2, and carboxypeptidase E (CPE) can lead to β-cell stress and hyperproinsulinemia, both of which are features of type 2 diabetes. "
11/02/2023 - "Proinsulin processing includes removal of several C-terminal basic amino acids and is performed principally by the exopeptidase carboxypeptidase E (CPE), and mutations in CPE or other prohormone convertase enzymes (PC1/3 and PC2) result in hyperproinsulinemia. "

07/01/2011 - "Defects in insulin processing enzymes including prohormone convertases 1/3 and 2, and carboxypeptidase E (CPE) can lead to β-cell stress and hyperproinsulinemia, both of which are features of type 2 diabetes. "
07/01/1999 - "To explore the role of chronically elevated free fatty acids (FFAs) in the pathogenesis of the hyperproinsulinemia of type 2 diabetes, we have investigated the effect of FFAs on proinsulin processing and prohormone convertases PC2 and PC1/PC3 in MIN6 cells cultured in Dulbecco's modified Eagle's medium with or without 0.5 mmol/l FFA mixture (palmitic acid:oleic acid = 1:2). "
11/02/2023 - "Proinsulin processing includes removal of several C-terminal basic amino acids and is performed principally by the exopeptidase carboxypeptidase E (CPE), and mutations in CPE or other prohormone convertase enzymes (PC1/3 and PC2) result in hyperproinsulinemia. "

01/01/1992 - "Both regimens cause basal hyperinsulinemia but normalize the hyperproinsulinemia observed during failure of oral agent therapy. "
10/01/1997 - "Neither sulfonylurea nor insulin therapy altered the relative hyperproinsulinemia. "
10/01/1997 - "Failure to improve the relative hyperproinsulinemia of NIDDM, despite significant reduction of hyperglycemia with exogenous insulin therapy, supports the hypothesis that relative hyperproinsulinemia in NIDDM is a reflection of a primary beta-cell defect rather than being secondary to hyperglycemia."
10/01/1997 - "Relative hyperproinsulinemia of NIDDM persists despite the reduction of hyperglycemia with insulin or sulfonylurea therapy."
05/01/1977 - "These results, which are comparable to those obtained by the more laborious column chromatography, could be summarized as follows: (1) proinsulin values in lean, young normal subjects do not vary greatly in response to insulin secretagogues; (2) proinsulin secretion in response to glucose results in a greater percentage of proinsulin in the older age group than in the younger group; (3) in lean adult and juvenile diabetic patients, the percentage of proinsulin is not excessive, whereas obese diabetics and pregnant diabetics appear to secrete relatively greater proinsulin than their diabetic controls; and (4) whereas most hyperinsulinemic states (Cusing's syndrome, adult-onset diabetics, acromegaly, and glucocorticoid therapy) are not associated with an increase in percentage of proinsulin, hyperinsulinemia of insulinoma, selected cases of functional hypoglycemia, and genetic hyperproinsulinemia are associated with a greater percentage of proinsulin. "

11/01/2018 - "An alternative way to investigate the relation between relative hyperproinsulinemia and increased secretory demand is to study the dynamic changes in the proinsulin-to-insulin ratio after partial pancreatectomy, a model of acute increased β-cell workload on the remaining pancreas. "

11/01/1998 - "From these findings, we conclude that pancreas-kidney transplantation provokes proportional hyperproinsulinemia, which is closely associated with its reduced clearance in the kidneys."
12/01/1993 - "Evidence that fasting hyperproinsulinemia after combined pancreas-kidney transplantation diminishes over time."

10/01/1997 - "The diabetic subjects on diet therapy had relative hyperproinsulinemia, assessed relative to C-peptide concentrations, fasting and in response to hyperglycemic clamping and arginine, compared with control subjects. "
10/01/1997 - "A similar trend was evident with fasting C-peptide concentrations with a reduction from 0.9 (0.6-1.4) nmol/l on diet therapy to 0.6 (0.4-0.9) nmol/l (P = 0.06), so that the relative hyperproinsulinemia, assessed as the ratio of fasting proinsulin to C-peptide, was unchanged by insulin. "