Acute Insulin Response to Glucagon, Tolbutamide, and Glucose in Non-insulin-dependent Diabetes of the Young

Naidoo, C; Jialal, Ishwarlal; Suleman, Amer; Rajput, M. C.; Joubert, S. M.

doi:10.2337/diacare.9.1.57

Cited by 10 publications

(3 citation statements)

References 10 publications

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“…These diabetic rats exhibited a specific failure of insulin release in response to glucose coexisting with a relative preservation of the responses to other secretagogues [17]. Such a pattern resembles that shown in some studies of human Type 2 diabetes [18][19][20] and is also charcteristic of Type1 diabetes in the early stage of the disease [21] and of Type 2 diabetes of the young [22]. This study was designed to determine if short-term (1 day) or long-term (30 days) oral gliclazide treatment modifies the pancreatic insulin content and the in vitro B-cell response to secretagogues (glucose, arginine and gliclazide) using the isolated perfused pancreas technique.…”

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confidence: 48%

Long-term gliclazide treatment improves the in vitro glucose-induced insulin release in rats with Type 2 (non-insulin-dependent) diabetes induced by neonatal streptozotocin

1989

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Summary. Neonatal rats treated with streptozotocin on the day of birth (n0-STZ) or on day 5 (n5-STZ) exhibited when fully grown a very mild or frank basal hyperglycaemia respectively and a specific failure of insulin release in response to glucose. To determine whether short (1 day) or long-term (30 days) gliclazide treatment modifies the pancreatic insulin content and the B-cell response to secretagogues, diabetic rats were given oral gliclazide (10 mg/kg per day) and compared to control diabetic and non-diabetic rats. Insulin secretion in the isolated perfused pancreas was studied the day after the last gliclazide administration. In severely hyperglycaemic n5-STZ rats (plasma glucose levels > 16 mmol/1) long-term gliclazide treatment did not lower the plasma glucose values, did not affect the pancreatic insulin stores, nor did it significantly modify the insulin release in vitro in response to glucose or arginine. In moderately hyperglycaemic n5-STZ rats (plasma glucose levels <16retool/I) the plasma glucose levels declined progressively reaching 8 mmol/l as a mean at the end of the gliclazide therapy. In the n5-STZ rats responsive to gliclazide the pancreatic insulin stores were increased twofold as compared to values in untreated n5-STZ rats, however, this difference did not reached significance and the pancreatic insulin stores in the responsive gliclazide treated rats remained depleted by 76% compared to normal insulin stores. In the n0-STZ rats (very mild hyperglycaemia) the long-term gliclazide treatment did not significantly modify the plasma glucose levels or the pancreatic insulin stores. After the 30-day gliclazide therapy in both the n5-STZ gliclazide responder group and the n0-STZ group: (1) the in vitro glucose-induced insulin secretion was increased three to fivefold, (2) the response to arginine which was basically increased in the untreated diabetic rats was again amplified two to threefold, (3) the insulin release in resp, onse to gliclazide was unchanged. In conclusion, long-term gliclazide therapy augments stimulated insulin secretion in these two rat models of Type 2 (non-insulin-dependent) diabetes and does not induce any refractoriness to acute sulfonylurea stimulation. The improvement of Bcell function observed here was not related to the concomitant variations of hyperglycaemia and/or pancreatic insulin content

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supporting

confidence: 48%

Long-term gliclazide treatment improves the in vitro glucose-induced insulin release in rats with Type 2 (non-insulin-dependent) diabetes induced by neonatal streptozotocin

1989

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“…Different secretagogues act at different sites [19,20]. Our patient clearly demonstrated inappropriately low C-peptide levels when his blood sugar levels were abnormally high, and this is what matters for normal glucose homeostasis.…”

Section: Discussionmentioning

confidence: 81%

Maturity Onset Diabetes of the Young in a Saudi Child: Case Report and Review of the Literature

et al. 1991

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Maturity onset diabetes of the young (MODY) is an autosomal dominant subtype of non-insulin-dependent diabetes mellitus that occurs at a young age. The patient may be asymptomatic, but if he is symptomatic, it usually takes the form of hyperglycemia with no ketosis. We describe a child whose history, physical findings, and results of investigations are consistent with the diagnosis of MODY. To the best of our knowledge, MODY has never been reported in the Saudi Arabian population. Case ReportA 10-year-old boy presented to the pediatric clinic with a history of nocturnal enuresis of six months' duration. The family first noticed that the child, who had previously been completely dry for the night, started to wet his bed almost every night. They thought it was due to the cold weather, as it started during winter time, but the symptoms persisted. He admitted that his drinking and voiding habits had increased slightly over the same period. His appetite and weight did not change. In the clinic he was found to have hyperglycemia (random blood sugar, 23.9 mmol/L; fasting blood sugar, 12.6 mmol/L). He was not dehydrated or acidotic. His urine, which was 4+ for sugar, was negative for ketones, so he was admitted for further investigation and management. He gave no history of infections especially immediately prior to the beginning of his symptoms. Other than tonsillectomy at the age of five years, past history was normal.Family history was very important, in that both parents are first-degree cousins and both are diabetics. The diabetes in his father, who was 55-years-old, had been diagnosed four years earlier, and he was on oral hypoglycemics. His mother, who was 48-years-old, had been diagnosed as having NIDDM when she was 35-yearsold. She had been on oral hypoglycemic agents for eight years, but changed to insulin five years ago. NIDDM had been diagnosed in his 30-year-old, eldest brother when he was 28 years old, and he had been on oral hypoglycemic agents since then. None of the remaining seven older siblings had any symptoms suggestive of diabetes, but unfortunately, they all refused to be screened. NIDDM was also found in his maternal grandparents, but the age of onset of their diabetes was not certain. His maternal grandmother, who had used oral hypoglycemic agents, had been on insulin for the last few years. His grandfather had died a few years earlier, but the cause of death was not known. On his father's side, only his father's cousin was diabetic and treated with oral agents.Examination revealed a normal-looking obese boy who was in no distress. He weighed 59.4 kg (> 95%) and was 149 cm tall (95%). His vital signs were normal; in particular, he was not tachypneic and there was no acetone odor to his breath. Remaining findings from general examination were essentially normal. During his hospitalization, his hyperglycemia was confirmed repeatedly, but urine remained ketone-free. His complete blood count, blood gas values, serum electrolyte concentrations, and lipid profile were within normal limits. His T3, T4,...

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“…Earlier data (15) clearly demonstrate hyperinsulinism in ''NIDDY'' patients, 75% of whom had a parent affected with diabetes. In MODY patients from the South Asian Indian peninsula, hyperinsulinemic responses to oral glucose were recorded (159), although there was loss of first phase insulin response to intravenous glucose administration (160). Insulin resistance in Indian NIDDY children was reported (161) and defects in insulin secretion and insulin action in MODY twins were recognized (162).…”

Section: Clinical and Metabolic Characteristics Of The Mody Syndromesmentioning

confidence: 99%

Molecular and biochemical analysis of the MODY syndromes

Winter

2000

Pediatric Diabetes

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Maturity onset diabetes of the young (MODY) is characterized by youth-onset diabetes that is inherited in an autosomal dominant (monogenic) pattern. Classic MODY accounts for less than 5% of cases of childhood diabetes in Caucasians, presents prior to age 25 years, is nonketotic, and may not require insulin treatment. A variant form of MODY that lacks a clearly defined genetic basis occurs in African Americans [atypical diabetes mellitus (ADM)] clinically presents more acutely and is initially insulin requiring. To date, five molecular causes of classic MODY have been identified: hepatocyte nuclear factor-4 alpha (HNF-4 alpha; MODY1), glucokinase (MODY2), hepatocyte nuclear factor-1 alpha (HNF-1 alpha; MODY3), insulin promoter factor-1 (IPF-1, MODY4), and hepatocyte nuclear factor-1 beta (HNF-1 beta; MODY5). MODY is studied as a model of beta cell hypofunction and modest insulinopenia. Clinical recognition of ADM is important for patient management to avoid confusion with type 1 diabetes mellitus.

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Acute Insulin Response to Glucagon, Tolbutamide, and Glucose in Non-insulin-dependent Diabetes of the Young

Cited by 10 publications

References 10 publications

Long-term gliclazide treatment improves the in vitro glucose-induced insulin release in rats with Type 2 (non-insulin-dependent) diabetes induced by neonatal streptozotocin

Long-term gliclazide treatment improves the in vitro glucose-induced insulin release in rats with Type 2 (non-insulin-dependent) diabetes induced by neonatal streptozotocin

Maturity Onset Diabetes of the Young in a Saudi Child: Case Report and Review of the Literature

Molecular and biochemical analysis of the MODY syndromes

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