The characteristics of blood glucose fluctuations in patients with fulminant type 1 diabetes mellitus in the stable stage

ABSTRACT Objective: The aim was to characterize blood glucose fluctuations in patients with fulminant type 1 diabetes (FT1DM) at the stable stage using continuous blood glucose monitoring systems (CGMSs). Subjects and methods: Ten patients with FT1DM and 20 patients with classic type 1 diabetes mellitus (T1DM) (the control group) were monitored using CGMSs for 72 hours. Results: The CGMS data showed that the mean blood glucose (MBG), the standard deviation of the blood glucose (SDBG), the mean amplitude glycemic excursions (MAGE), the blood glucose areas and the percentages of blood glucose levels below 13.9 mmol/L were similar between the two groups. However, the percentage of blood glucose levels below 3.9 mmol/L was significantly higher in the FT1DM group compared to the T1DM group (p < 0.05). The minimum (Min) blood glucose level in the FT1DM group was significantly lower than that of the T1DM group (p < 0.05). Patients with FT1DM had severe dysfunction of the islet beta cells and alpha cells compared to patients with T1DM, as indicated by lower C-peptide values and higher glucagon/C-peptide values. Conclusion: In conclusion, patients with FT1DM at the stable stage were more prone to hypoglycemic episodes as recorded by CGMSs, and they had a greater association with severe dysfunction of both the beta and alpha islet cells compared to patients with T1DM.

Improving Effect of the Acute Administration of Dietary Fiber-Enriched Cereals on Blood Glucose Levels and Gut Hormone Secretion

Dietary fiber improves hyperglycemia in patients with type 2 diabetes through its physicochemical properties and possible modulation of gut hormone secretion, such as glucagon-like peptide 1 (GLP-1). We assessed the effect of dietary fiber-enriched cereal flakes (DC) on postprandial hyperglycemia and gut hormone secretion in patients with type 2 diabetes. Thirteen participants ate isocaloric meals based on either DC or conventional cereal flakes (CC) in a crossover design. DC or CC was provided for dinner, night snack on day 1 and breakfast on day 2, followed by a high-fat lunch. On day 2, the levels of plasma glucose, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), and insulin were measured. Compared to CC, DC intake exhibited a lower post-breakfast 2-hours glucose level (198.5±12.8 vs. 245.9±15.2 mg/dL, P<0.05) and a lower incremental peak of glucose from baseline (101.8±9.1 vs. 140.3±14.3 mg/dL, P<0.001). The incremental area under the curve (iAUC) of glucose after breakfast was lower with DC than with CC (P<0.001). However, there were no differences in the plasma insulin, glucagon, GLP-1, and GIP levels. In conclusion, acute administration of DC attenuates postprandial hyperglycemia without any significant change in the representative glucose-regulating hormones in patients with type 2 diabetes (ClinicalTrials.gov. NCT 01997281).

Delayed Response of Amylin Levels after an Oral Glucose Challenge in Children with Prader-Willi Syndrome

PURPOSE: Amylin secretion is increased parallel to insulin in obese subjects. Despite their marked obesity, a state of relative hypoinsulinemia occurs in children with Prader-Willi syndrome (PWS). Based on the hypothesis that amylin levels may be relatively low in PWS children, contributing to their excessive appetite, we studied amylin levels after oral glucose loading in children with PWS and overweight controls. MATERIALS AND METHODS: Plasma levels of amylin, glucagon, insulin, and glucose were measured at 0, 30, 60, 90, and 120 min after a glucose challenge in children with PWS (n = 18) and overweight controls (n = 25); the relationships among the variables were investigated in these two groups. RESULTS: Amylin levels were significantly correlated with insulin during fasting and during the oral glucose tolerance test in both groups. Amylin levels between 0 and 60 min after glucose loading were statistically different between the two groups. They were lower in children with PWS than in the controls between 0 and 30 min after glucose loading. CONCLUSION: The relatively low levels of amylin, compared to those in overweight controls, during the early phase of glucose loading in patients with PWS, may contribute, in part, to the excessive appetite of PWS patients as compared to the overweight controls.

Implicações clínicas da persistência de anti-GAD positivo e peptídeo C detectável em pacientes com diabetes melito tipo 1 de longa duração / GADA persistence and detectable C peptide in patients with long standing diabetes mellitus type 1

OBJETIVO: Avaliar se anti-GAD positivo e PC detectável se correlacionam com a presença de outras doenças autoimunes, com controle glicêmico e com risco de retinopatia no diabetes melito tipo 1 (DMT1) > 3 anos de duração. PACIENTES E MÉTODOS: Cinquenta sujeitos com DMT1 foram entrevistados, realizaram fundoscopia e dosaram PC pré e pós-glucagon, HbA1C e anti-GAD. RESULTADOS: Pacientes anti-GAD+ (n = 17) apresentaram maior frequência de doenças autoimunes em relação aos demais (p = 0,02). PC detectável (n = 11) também foi associado ao aumento dessa prevalência (p = 0,03), porém nenhum dos dois parâmetros influenciou na presença de retinopatia diabética. PC detectável não influenciou no controle glicêmico (HbA1C média) (p = 0,28), porém as doses diárias de insulina foram mais baixas (0,62 vs. 0,91 U/kg/dia; p = 0,004) neste grupo. CONCLUSÃO: Apesar de não ser um marcador para outras doenças autoimunes, o anti-GAD+ parece ser não só um sinalizador de autoimunidade pancreática. PC detectável também parece ter papel promissor na detecção dessas comorbidades. Ambos não interferiram na presença de retinopatia, entretanto, o PC detectável se relacionou a menores necessidades de insulina.

OBJECTIVE: The aim of this study was to evaluate if GADA+ and detectable CP had any influence in other autoimmune diseases, glycemic control, and risks of retinopathy in diabetes mellitus type 1 (T1DM) lasting longer than 3 years of duration. SUBJECTS AND METHODS: Fifty T1DM subjects were interviewed, performed fundoscopic examination, and measured CP before and after glucagon, HbA1C, and GADA. RESULTS: GADA+ (n = 17) had a higher frequency of other autoimmune diseases when compared to GADA (p = 0.02). Detectable CP was also associated with a higher prevalence of these diseases (p = 0.03), although, retinopathy was not influenced by either one. Detectable CP had no influence in the glycemic control (mean HbA1C) (p = 0.28). However, insulin daily doses were lower in this group (0.62 vs. 0.91 U/kg/day; p = 0.004). CONCLUSION: Although not recommend as a marker of other autoimmune diseases, GADA+ seems to be not only a pancreatic autoimmunity signal. Detectable CP may also have some promising influence in detecting these diseases. Neither influenced the presence of retinopathy, but insulin daily requirements were smaller when CP was present.

[Effect of GABA on plasma cytokine concentration and beta and alpha cell mass in CD1 diabetic mice]

Type I diabetes is an autoimmune disease associated with T lymphocytes function in beta cells. This process can increase cytokine secretion, which can cause beta cell inflammation and death. Since GABA, [y-aminobutyric acid] is a major inhibitory neurotransmitter, and low concentration of GABA can increase cytokine secretion, the aim of this study was demonstrate to the inhibitory effect of GABA administration on cytokine secretion and decrease in beta cell death and also to show the ability of beta cells in insulin secretion. Seven week old CD1 mice were used. To induce diabetes, animals received 40 mg/kg of STZ five days continuously. Two months later, animals were divided into two groups, one receiving 200 micromole of GABA and the other [controls] the same volume of PBS for 10 weeks. Serum glucagon levels, and alpha cells significantly decreased in the [IL12 IL1beta, TNF alpha] mass and some cytokine levels in the GABA group. Plasma insulin level and beta cell mass significantly increased in comparison to the control group. From the results of this study we conclude that GABA administration causes inhibition in cytokine secretion, improves beta cell mass and increases insulin secretion. May be, in the future, if GABA shows no side effects we can use GABA for type one diabetes

role of nitric oxide synthase in post-operative hyperglycaemia

Post-operative hyperglycaemia is important with regard to outcomes of surgical operations. It affects postoperative morbidity, length of hospital stay, and mortality. Poor peri-operative blood glucose control leads to a higher risk of post-operative complication. Insulin resistance as a cause of post-operative hyperglycaemia has been blamed for some time. Nitric Oxide [NO] is produced by nitric oxide synthase [NOS] isoenzymes. Inducible nitric oxide synthase [iNOS] is not a normal cellular constitute. It is expressed by cytokines and non-cytokines e.g. fasting, trauma, intravenous glucose, and lipid infusion, which are encountered in surgical operations. Review of current published data on postoperative hyperglycaemia was completed. Our studies and others were explored for the possible role of NO in this scenario. Induction and expression of iNOS enzyme in pancreatic islet cells is included in the chaotic postoperative blood glucose control. The high concentrations of iNOS derived NO are toxic to pancreatic p-cells and may inhibit insulin secretion postoperatively. Hence, current peri-operative management is questionable regarding post-operative hyperglycaemia and necessitates development of a new strategy

Study of pancreatic islet cell function in cirrhotic patients due to hepatitis C virus

The liver is of key importance in the proper functioning of most of endocrine system. It is a major organ for metabolic degradation of many hormones. In chronic liver disease, there is a change in the concentrations of main pancreatic hormones. In this study, we aimed to study pancreatic islet cell hormones in non ascitic non diabetic cirrhotic HCV patients by measuring these hormones basally and after intravenous glucose load with different concentrations to evaluate pattern of endocrine pancreatic hormonal response at increasing glucose concentration. This case-control study included 25 non ascitic non diabetic patients with cirrhosis due to HCV infection; age ranged from 28 to 60 years. They were selected from outpatient clinic of National Hepatology and Tropical Medicine Research Institute [NHTMRI] during June 2004 to January 2005. Fifteen age and sex matched apparently healthy control subjects from same area were also included in study. Assessment of pancreatic islet cell function was done by assaying insulin, C-peptide, somatostatin and glucagon hormones. All hormones were determined by radioimmunoassay [RIA] for both patients and controls. Basal insulin, basal somatostatin and basal glucagons levels were significantly higher than that of controls [p<0.05]. Basal C-peptide was significantly lower than that of controls [p<0.05]. After intravenous glucose load with different concentrations 5%, 10% and 25%, insulin level showed a significant increase than controls [p<0.05], while other hormones showed no significant difference as compared to controls [p>0.05]. Pancreatic islet cell functional defects with liver cirrhosis due to HCV infection

Insulin and glucagon ratio in the patho-physiology of diabetic ketoacidosis and hyperosmolar hyperglycemic non-ketotic diabetes

To assess the role of insulin / glucagon ratio in pathophysiology of diabetic ketoacidosis and hyperosmolar hyperglycemic non-ketotic diabetes. Case control, analytical study. Military Hospital, Rawalpindi from September 2003 to August 2004. The study included 7 patients with diabetic ketoacidosis, 3 patients with hyperosmolar hyperglycemic non-ketotic diabetes, 8 patients with uncontrolled type 1 diabetes mellitus and 12 patients with uncontrolled type 2 diabetes mellitus. Twenty non-diabetic persons having blood glucose level less than 6 mmol/L were selected as control group. Patients' detailed history was taken and general physical examination was done. Plasma samples of all the patients and control subjects were assayed for plasma glucose, glycosylated hemoglobin, plasma insulin and glucagon levels. Presence or absence of ketone bodies in urine was also determined. Seven patients with diabetic ketoacidosis, 3 females and 4 males, were found to be hyperglycemic [p < 0.001], hypoinsulinemic [p < 0.05] and hyperglucagonemic [p < 0.001] as compared to control group. Three patients with hyperosmolar hyperglycemic non-ketotic diabetes, 1 male and 2 females, were hyperglycemic [p < 0.001]. Eight patients with uncontrolled type I diabetes mellitus, 6 males and 2 females, were having hyperglycemia [p< 0.001] along with hyperglucagonemia [p < 0.001]. Twelve patients with uncontrolled type 2 diabetes mellitus, 6 males and 6 females, were found to be hyperglycemic [p < 0.001] and hyperinsulinemic [p < 0.001] as compared to control group. The insulin / glucagon ratio was found to be 1: 0.9 in diabetic ketoacidosis, 1: 0.15 in hyperosmolar hyperglycemic non-ketotic diabetes, 1: 0.24 in type 1 diabetics, 1: 0.08 in type 2 diabetics, and 1: 0.1 in the control group. It was concluded that if insulin / glucagon ratio in type 2 diabetics reduces to 1: 0.9 then these patients may develop ketoacidosis instead of hyperosmolar hyperglycemic non ketotic diabetes. Hence, it is the balance and interplay of insulin and glucagon which predicts the type of acute hyperglycemic emergencies [diabetic ketoacidosis and hyperosmolar hyperglycemic non-ketotic diabetes] being observed in diabetic patients and not the type of diabetes mellitus

Comparative study between the perioperative and catabolic effects of epidural levobupivacaine and ropivacaine

Increased whole body protein breakdown and amino acid oxidation resulting in nitrogen loss, are typical features of altered protein homeostasis after surgery. Because protein represents both structural and functional components extensive loss of lean and tissue mass may cause delayed wound healing, compromised immune function and muscle weakness leading to prolonged convalescence and morbidity, neuro-axial blockade with epidural local anesthetics has been demonstrated to attenuate catabolic response to major abdominal surgery. The aim of this study is to compare the ant catabolic affect of levobupivacaine, ropivacaine and general anesthesia by the perioperative kinetics of blood ureaglucose, and hormones as glucagons, insulin, cortisol, and metabolites as lactate. Thirty patients with bladder cancer, scheduled for elective cyst prostatectomy followed by elective reconstruction of the bladder with small bowel after informed consent, patients were divided into 3 groups, each 10 patients, the first group was received general anesthesia, group II epidurally levobupivacaine was used, group III ropivacaine was used epidurals. Levobopivacaine was 0-5%, while ropivacaine was used, postoperative infusion epidurally was prepared as 5ml/hour and with 2ml increment a lockout time of 20 minutes, and levobupivacaine group was received 0.125% solution concentration, while ropivacaine was received at a higher concentration 0.2%. Blood samples were taken one before induction of general anesthesia or injection of local anesthetic, the second intraoperatively and 3 blood samples at the 3days postoperatively. All sample [5ml each were immediately centrifuged at 4 C and the plasma stored at -70Co until analysis. Ureaglucose, lactate, hormones [insulin, glucagons, cortisol] were determined, plasma concentrations of glucose, lactate were determined enzymatically. Insulin, glucagons and cortisol were quantified with radioimmunoassay. There was significant increase in blood sugar in group I in the first and second day postoperatively it was 150 +/- 20, 150 +/- 30respectively, there was significant in crease in insulin concentration in group II, III in the second day postoperatively it was 57 +/- 20, 80 +/- 15 respectively, and in the third day postoperatively, it was 90 +/- 25, 95 +/- 20respectively. There was significant decrease in insulin level in group I during surgery and in the first, second day postoperatively. It was 29 +/- 18, 30 +/- 30, 30 +/- 20 respectively. There was significant increase in glucagons level in group I in the third day postoperatively; it was 10 +/- 3. Blood urea level was significantly lower in group II and III in third day postoperatively. Blood cortisol was significantly increased in the 1st and second day postoperatively in group I. The study concluded that postoperative epidural levobupivacaine or ropivacaine have nearly equally attenuate the catabolic response after major abdominal surgery, by preventing postoperative protein breakdown with out affecting glucose metabolism

Effect of insulin-induced hypoglycaemia on plasma pancreatic polypeptide and glucagon levels in conscious dogs

The aim of the present study has been to identify the role of nitric oxide [NO] in mediating pancreatic endocrine responses to severe hypoglycaemia [2.0 nmol/kg insulin I.V.] in conscious dogs. The experiments were carried out on 18 apparently healthy adult male conscious dogs divided into three groups: Group I: Six dogs sacrificed as control group. Group II: Six dogs subjected to severe hypoglycaemia in the absence of L-NAME [NOS blocker] and sodium nitroprusside [NO donor]. Group III: Six dogs subjected to severe hypoglycaemia in the presence of L-NAME [100 mg/kg I.A.] and sodium nitroprusside [2-4 micro g/min/kg I.V.].Glucose was measured by means of a Mark 2 Beckman Glucose Analyser, Glucagon and PP were easured by radioimmunoassay. Determination of cGMP levels was studied using pancreatic tissues from the three studied groups. Administration of L-NAME effectively produced a significantly reduced plasma pancreatic polypeptide [PP] response. In contrast, the glucagon response was not significantly affected. Moreover, plasma glucagon values were consistently higher in group III [with L- NAME] when compared to group II [without L-NAME] at 30 and 120 min. intervals, [t = 5.36, P < 0.001, and t = 6.32, P< 0.001 respectively]. One can conclude that, in the absence of L-NAME, production of NO may contribute to the PP response, but not to the glucagon response to hypoglycaemia in this species under physiological conditions, in this study, there was a significant increase in pancreatic tissue cGMP in the studied dogs without L-NAME and sodium nitroprusside as compared to both control dogs [t= 11.6, P < 0.001], and those receiving L-NAME and sodium nitroprusside [t = 8.25, P < 0.05]. This explains a possible rote of cGMP in the process of PP release through NO gas. Conclusions. Administration of NOS blocker has produced a significantly reduced plasma pancreatic polypeptide [PP] response with no significant effect on glucagon secretion during insulin-induced severe hypoglycaemia in conscious dogs. cGMP has been found to play a possible role in the process of PP release through NO gas

Plasma insulin/glucagon molar ratio in euglycaemic experimental animals: effect of nifedipine

To evaluate the plasma levels of insulin and glucagon as well as insulin/glucagon molar ratio under the effect of calcium-channel blocker [nifedipine] in adult male albino rats. Adult male albino rats were classified into placebo [acute and chronic] and nifedipine-treated [acute and chronic] groups. The drug groups received nifedipine in recommended daily doses by means of intragastric tubes for three months for the chronic group whereas the acute group received nifedipine in a single dose. Insulin and glucagon were assayed by RIA Kits and insulin/glucagon [I/G] ratio was calculated. A decrease in plasma levels of insulin and an increase in plasma levels of glucagon together with decrease in insulin/glucagon molar ratio were recorded in chronic nifedipine group as compared to placebo group. The calcium-channel blockers have a hyperglycaemic effect which is thought to be time dependent and so a great care must be taken into consideration if these drugs are obliged for the chronic use for diabetic and hypertensive patients and plasma glucose level as well as I/G ratio should be monitored regularly in patients receiving calcium-channel blocker-nifedipine

Disfunçäo pancreática endócrina e exócrina em etilistas assintomáticos / Endocrine and exocrine pancreatic dysfunction in asymptomatic alcoholics

O autor estudou a funçäo pancreática numa populaçäo de 131 etilistas assintomáticos e em 102 indivíduos sadios (controle). O estudo da funçäo pancreática exócrina realizado através de estímulo com secretina mais colecistocinina revelou, além do aumento de volumem hipersecreçäo de bicarbonato, proteínas totais e albumina no suco pancreático dos etilistas. A avaliaçäo da funçäo endócrina através de estímulo com glicose via oral e IV e arginina IV revelou glicemias normais e níveis diminuídos de insulina e peptídeo C séricos, indicando hipofunçäo das células beta do pâncreas. Estes achados caracterizam disfunçäo pancreática endócrina e exócrina em etilistas assintomáticos

Congenital generalized lipodystrophy, a case report.

Generalized lipodystrophy is a rare condition which can be divided into congenital and acquired types, based on the age at presentation and pattern of inheritance. The congenital type of generalized lipodystrophy or Lawrence-Seip syndrome presents in first two years of life and is inherited in an autosomal recessive pattern. The diagnosis is made on the basis of loss of body fat, muscular hypertrophy, acanthosis nigricans, hirsutism, hepatomegaly with fatty liver, hyperlipidemia and hyperglycemia with insulin resistance. A 2 1/2-year-old Thai girl with the clinical features of Lawrence-Seip syndrome is reported. Abnormal platelet function was detected in this girl.

[ brief revision on the functions of the NPY in the body]

Neuropeptide Y [NPY] is a 36 amino-acid residue peptide of pancreatic polypeptide family, which shares considerable sequence homology with PYY. It was originally isolated from porcin brain by Tatemoto et al in 1982, which is now known to be distributed throughout central and perpheral nervous systems of various species examined to date. It occurs in mammalian brain in higher concentration than all other peptides studied. It has been suggested that NPY and PYY are involved in the autonomic regulation of insulin and glucagon release. Any alteration in plasma level of the two hormones, could suggest a possible mode of action of the brain neuropeptide on the peripheral organ, specifically the islet of langerhans. NPY projections from the arcuate to medial preoptic area may be related to the central effects of this neuropeptide on luteinizing hormone release and sexual behaviour. Increasing evidence suggests a role for NPY cerebral and coronary vasospasm. The dense plexus of NPY terminal around cerebral vessels are probably responsible for NPY's potent vasoconstriction in the cerebral cortex. Coronary vesseles are also innervated heavily by NPY terminals, indicating a role for this neuropeptide in pathogenesis of coronary vasospasm. In addition, NPY affects both physiological systems and endocrine that modulate energy balance and metabolism. There are abundant evidence, particularly in rat for the involvement of NPY in the control of feeding behaviour. For example intracerebroventricular [ICV] injection of NPY, produces a strong orexigenic effect which is more enhanced by microinjection of the substance directly into the paraventricular nuclei [PVN] of the hypothalamus which receives a dense innervation of NPY containing neurons. Repeated central administration of NPY leads to continuous hyperphagia which persits, despite massive gastrointestinal distension. Existing evidence suggests that central neurochemical mechanisms involve for controlling the intake of macronutrients. In this respect it has been shown that NPY would preferentially stimulates carbohydrates and with a lesser extent fat ingestion, which develop the obesity with no significant potentiation of protein consumption. The evidences are consistant with a role for NPY in hypothalamic controle of macronutrient intake and body weight regulation, and suggest that disturbances in brain NPY may contribute to the development of eating and weight disturbances. Finally there seems to be a negative relationship between NPY and CCK petides, which is not surprising, given their opposite role in the control of feeding

Criteria of an experimental model analogous to type I human diabetes mellitus

Three doses of streptozotocin were given to adult male Boskat rabbits on 3 successive days as 20 mg/kg/day [i.v.]. The experimental follow up was extended to one month after completion of the treatment schedule. At the 14th day, there was a pronounced glucosuria in 100% of the treated animals with ketonuria in 67% of them. After 30 days, there was a marked rise in fasting plasma glucose [111%] associated with a marked reduction [51%] in plasma insulin activity with respect to the matched control group. Blood lactate showed 21% increase, but blood pyruvate was unchanged, while liver glycogen content was decreased by 30%. The radioimmunoassay of plasma growth hormone [GH] and glucagon revealed 57% and 20% increases in their levels, respectively, in the streptozotocin-treated rabbits. However, plasma cortisol was unchanged in comparison with the control group. The picomolar plasma ratios of GH, glucagon and cortisol in relation to insulin showed significant increases by 220%, 143% and 95%, respectively, in the diabetic animals with respect to normal. The overall pattern of results revealed a prototype of chemically-induced diabetes analogous to the human juvenile one and characterized by sustained hyperglycemia, insulinopenia, glucosuria and ketonuria. An additional merit of this model is the close similarity and overlapping between the estimated normal values of test parameters in Boskat rabbits and the reported corresponding human values, except in case of liver glycogen, plasma GH and cortisol

Glucagon response to glucose load in offspring of conjugal type 2 diabetic parents in south India.

Immunoreactive glucagon responses were measured in 21 normoglycaemic adult offspring of non-insulin dependent (Type 2) diabetic parents, in the fasting state and during an oral glucose tolerance test. In 7 of the 21 offspring, the mean fasting immunoreactive glucagon value was significantly lower than the control value (p < 0.001). In this group, glucose stimulation did not produce inhibition of immunoreactive glucagon secretion. The insulin response in this group was not significantly different from the values in the other study groups. In the other 14 offspring, the pattern of glucagon response to glucose stimulation was similar to controls. It is likely that this non-suppressive effect of glucose on immunoreactive glucagon in some of the "prediabetic" individuals is an early change in the alpha cell function during the natural history of non-insulin dependent diabetes in Asian Indian subjects.

La relación insulina/glucagon en la remisión diabética espontánea / Insulin/glucagon relationship in spontaneous diabetic remission

Definimos como "remisión diabética" la suspensión del tratamiento insulínico por un período mayor de 15 días, luego de la normalización de as glucemias y desaparición de las glucosurias. Hemos estudiado 21 niños diabéticos insulino-dependientes en el período de remisión (10 niños y 11 niñas) y 29 niños normales como control. Dos clases de pruebas fueron realizadas: glucosa intravenosa (GEV) y glucosa post-tolbutamida (GPT). Se separaron dos grupos en los niños que efectuaron la prueba de GEV. En uno se dosó glucosa, insulina, somatotrofina y glucagon plasmáticos y en el otro se determinó glucosa y péptido-C. La glucemia fue menor en los normales que en los niños en remisión. La desaparicióon de la glucosa (constante "K") fue máas alta en los normales (p < 0,001) indicando claramente el hipoinsulinismo hallado. La secreción de insulina lluego de ;a glucosa EV fue muy baja en el grupo en remisión, no pasando del valor basal. Solo dos niñas mostraron un valor normal o alto luego de la sobrecarga de glucosa y una de ellas en uns egundo estudio mostró el hipoinsulinismo común del grupo diabético en remisión. La cinética de la secreción de glucagon y somatotrofina en elg rupo en remisión fue normal, pero los niveles de glucagon fueron bajos. Cuando el área integrada (0-120 min) fue determinada para la insulina, somatotrofina y glucagon, se observó que la insulina y el glucagon eran bajos en relación a los normales (p < 0,05) y la somatotrofina igual. Sin embargo , la relación insulina/glucagon fue similar en ambos grupos. El péptido-C en la prueba de GEV mostró en los niños en remisión un valor menor que en el grupo normal semejando el comportamiento del otro grupo en remisión en donde se dosó la insulina. Durante la prueba de glucosa psot-tolbutamida, el grupo normal respondió con un pico de secreción de insulina en cada estímulo, siendo mayor la respuesta a la glucosa post-tolbutamida. En el grupo en remisión, la glucemia fue más elevada que en el grupo normal y la secreción de insulina no sobrepasó el nivel basal luego de los estímulos. La secreción de la somatotrofina en la fase de glucosa fue mas baja que en los normales y el glucagon fue consistentemente menor en este grupo. Podemos concluir que los niños en remisión no presentan una velocidad de desaparición de glucosa normal, coincidente con un marcado hipoinsulinismo. El glucagon es proporcionalmente tan bajo como la secreción de insulina, lo que permite que el índice insulina/glucagon sea similar en lo

Reserva insulsinica en jovenes diabeticos con calcificaciones pancreáticas

Estudiamos la reserva de insulina a través de la determinación de péptido-C en suero, luego de estímulo con glucagón, en jóvenes diabéticos tropicales con calcificaciones pancreáticas, en diabéticos tipo I establecidos y en un grupo de jóvenes normales. Los diabéticos con calcificaciones pancreáticas mostraron cierta reserva de insulina, ya que sus concentraciones de peptido-C fueron superiores a las de los diabéticos tipo I, obtiniéndose diferencias significativas (p < 0.05) al comparar ambos grupos a los 10 y 15 minutos luego del estímulo con glucagón. La reserva de insulina de estos diabéticos con calcificaiones, sugiere la posibilidad de intentar lograr el control de estos casos con hipoglucemiantes orales o regulación dietética