Pre-Type I Diabetes: Linear Loss of Beta Cell Response to Intravenous Glucose

Srikanta, S.; Ganda, Om P; Gleason, Ray E.; Jackson, Richard A.; Soeldner, J S; Eisenbarth, George S.

doi:10.2337/diab.33.8.717

Cited by 156 publications

(96 citation statements)

References 5 publications

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“…Immediately thereafter, 0.5 g glucose per kg of body weight (maximum: 35 g) as a 40% aqueous solution was infused into the second cannula within 3 min±15 s. Serum insulin and C-peptide levels at time points 1 and 3 min were used for calculation of the first-phase insulin response (FPIR). The results were evaluated according to published standards [9,18].…”

Section: Testing Proceduresmentioning

confidence: 99%

Aetiological heterogeneity of asymptomatic hyperglycaemia in children and adolescents

et al. 2006

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We identified 35 carriers of GCK mutations causing MODY2, two carriers of TCF1 mutations causing MODY3, one carrier of a HNF4A mutation causing MODY1 and one carrier of a KCNJ11 mutation causing permanent neonatal diabetes mellitus. Of the remaining patients, 11 progressed to type 1 diabetes mellitus (T1DM) and 9 had impaired glucose tolerance or diabetes mellitus of unknown origin. In 23 subjects, an impairment of blood glucose levels was not confirmed. We conclude that 39 of 82 paediatric patients (48%) with randomly found fasting hyperglycaemia suffered from single gene defect conditions, MODY2 being the most prevalent. An additional 11 patients (13%) progressed to overt T1DM. The aetiological diagnosis in asymptomatic hyperglycaemic children and adolescents is a clue to introducing an early and effective therapy or, in MODY2, to preventing any future extensive re-investigations.

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Section: Testing Proceduresmentioning

confidence: 99%

Aetiological heterogeneity of asymptomatic hyperglycaemia in children and adolescents

et al. 2006

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“…The advantage of an intravenous test is the lack of influence of the entero-insulineric axis. The standard intravenous glucose tolerance test predominantly provides information about the early insulin secretion phase [16]. The GIT used in this study with our newly provided reference values, established in the same laboratory, accurately evaluated hyperinsulinemia induced by growth hormone therapy.…”

Section: Discussionmentioning

confidence: 99%

Glucose Tolerance and Insulin Secretion in Children before and during Recombinant Growth Hormone Treatment

Filler¹,

Amendt

Kohnert

et al. 1998

Horm Res Paediatr

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This study evaluates glucose metabolism and insulin secretion in children with Ullrich-Turner syndrome (UTS), chronic renal failure (CRF) and kidney transplantation (KTx) with rh GH therapy using an intravenous glucose infusion test. Before treatment, glucose AUC was significantly increased in all patient groups when compared to normal controls. Both the early and second phases of insulin secretion were not altered. During treatment, elevated glucose AUC showed a further increase in patients with KTx but not in patients with CRF or UTS. Both the early and second insulin secretion phases rose significantly in UTS and were transiently elevated after 6 and 12 months of therapy in patients with CRF and KTx. We conclude that growth hormone therapy aggravates alteration of glucose metabolism in patients with KTx and not in children with CRF and UTS. Progressive hyperinsulinemia occurred only in patients with UTS.

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“…The cystine content of leukocytes was normal. Using the method described by Srikanta et al [8], an IV glucose tolerance test (IVGTT) performed before rhGH treatment revealed normal glucose tolerance (k=2.65). Both early and total insulin secretion and reactive C-peptide production (actual Cpeptide concentration minus average baseline concentration before glucose infusion) were within the range of 15 control prepubertal patients with a similar degree of renal insufficiency (Fig.…”

Section: Case Reportmentioning

confidence: 99%

Reversible diabetes mellitus during growth hormone therapy in chronic renal failure

Filler

Franke

Amendt

et al. 1998

Pediatric Nephrology

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A 12-year-old girl with short stature due to idiopathic Fanconi syndrome and chronic renal failure was treated with recombinant human growth hormone (rhGH). There was no family history of diabetes mellitus and the glucose tolerance before treatment was normal. Intravenous glucose tolerance tests were performed before, during and after treatment. Two months after starting rhGH the early phase of insulin secretion (1-+3-min values) was diminished, and the patient developed manifest diabetes mellitus with hyperglycemia and an elevated hemoglobin A1c. Following discontinuation of rhGH, glucose tolerance slowly returned to normal.

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Pre-Type I Diabetes: Linear Loss of Beta Cell Response to Intravenous Glucose

Cited by 156 publications

References 5 publications

Aetiological heterogeneity of asymptomatic hyperglycaemia in children and adolescents

Aetiological heterogeneity of asymptomatic hyperglycaemia in children and adolescents

Glucose Tolerance and Insulin Secretion in Children before and during Recombinant Growth Hormone Treatment

Reversible diabetes mellitus during growth hormone therapy in chronic renal failure

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