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Results for “Glucose Intolerance”

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PubMedDate not supplied

[Study of the frequency of diabetes mellitus and glucose intolerance in patients with cystic fibrosis]

OBJECTIVE: To evaluate the frequency of diabetes mellitus and glucose intolerance in patients with cystic fibrosis treated at the Pediatric Gastroenterology Service of HC-FMRP-USP. METHODS: A cross-sectional analytical study was conducted on a group of 25 patients with mucoviscidosis who were followed up at HC-FMRP-USP. Oral glucose tolerance tests (OGTT) were performed, with simultaneous determination of glycemia and insulinemia. Areas under the curve were obtained for glycemia (G) and insulinemia (I) and the I/G ratio was calculated and correlated with the duration of clinical manifestation and pancreatic exocrine function. RESULTS: Five patients presented alterations: one was diabetic and four had glucose intolerance and/or hyperinsulinemia. There was a direct correlation between the area under the curve for insulinemia and the duration of mucoviscidosis. A significant inverse correlation was also observed between the area under the curve for insulinemia and I/G ratio, and number of enzyme capsules/kg/day. CONCLUSIONS: The frequency of alterations in glucose homeostasis observed in patients with mucoviscidosis was higher than in the population at large (20% of the total sample and 33% of the group of patients with glycemia and insulinemia on OGTT). Therefore, it is important that glucose tolerance tests be performed systematically in patients with mucoviscidosis so that metabolic abnormalities can be early detected, and proper treatment can be initiated.

Journal Article↗

PubMed1993

[Evaluation of the participation of proinsulin in hyperinsulinism in patients with obesity and glucose intolerance].

The comparison of the results of two insulin assays, a RIA using a polyclonal antibody and a EMIA using two monoclonal antibodies in blood samples collected during an oral glucose load in normal, obese, glucose intolerant and type II diabetic patients indicated that hyperinsulinemia of obese and glucose intolerant patients is not associated to increased proinsulin/insulin ratio.

Adult↗

PubMed1988

Control of spontaneous glucose intolerance, hyperinsulinemia, and islet hyperplasia in nonobese C3H.SW male mice by Y-linked locus and adrenal gland.

An inbred strain predisposition to maturity-onset impairment of glucose tolerance was discovered in C3H.SW/SnJ inbred male mice. Males were group-caged from weaning and subjected to repetitive handling stress; deterioration of glucose tolerance developed between 5 and 8 months of age in association with extreme hyperinsulinemia. Some males developed transient chemical diabetes in which plasma glucose concentrations were inappropriately high in relation to the high levels of plasma insulin. By 12 months of age, males previously glucose intolerant had regained a normal glucose tolerance. At death, a massive hypertrophy and hyperplasia of the islet beta-cells was documented in these mice. The impaired glucose tolerance could be circumvented by adrenalectomy at weaning. Although these finding suggested the presence of an obesity gene, the C3H.SW group-caged males were not obese when compared with C3HeB/FeJ males which, although moderately hyperinsulinemic, did not develop the glucose intolerance syndrome. Transfer of the Y chromosome from the C3HeB/FeChp background into the C3H.SW inbred background led to a reduction in the hyperinsulinemic and hyperglycemic stress on the pancreatic islets. Thus the extrinsic environment (caging and handling stress), mediated in part via the adrenal gland, could interact with sex-linked genetic susceptibility modifiers to stimulate hyperplasia of the pancreatic islets and produce a transient insulin resistant state of impaired glucose tolerance in the absence of obesity.

Adrenal Glands↗

PubMed1993

Insulin resistance, glucose intolerance, and hyperinsulinemia. Hypertriglyceridemia versus hypercholesterolemia.

Plasma glucose and insulin responses to oral glucose and mixed meals and the ability of insulin to stimulate glucose disposal were quantified in normal volunteer subjects and patients with types IIA, IIB, and IV hyperlipoproteinemia (HLP). The results indicated that patients with either type IIB or IV HLP had higher plasma glucose (p < 0.05-< 0.001) and insulin (p < 0.001) responses to both oral glucose and mixed meals compared with the normal subjects and patients with type IIA HLP. Steady-state plasma glucose concentrations (mmol/L) were also higher (p < 0.001) in patients with types IIB (13.3 +/- 0.6) and IV (12.8 +/- 1.2) HLP during a continuous infusion of somatostatin, glucose, and insulin than either the control group (volunteer subjects) (6.2 +/- 0.9) or patients with type IIA HLP (5.6 +/- 1.0). Because the steady-state plasma insulin concentrations were similar in all four groups, patients with either type IIB or IV HLP were resistant to insulin-mediated glucose uptake. These data indicate that patients with hypertriglyceridemia are insulin resistant, glucose intolerant, and hyperinsulinemic, irrespective of the plasma cholesterol concentration. The results further demonstrate that hypercholesterolemic patients with normal triglyceride concentrations do not have any abnormalities of glucose and insulin metabolism.

Adult↗

PubMed1996

[Pathogenesis and treatments of glucose intolerance with liver cirrhosis in men--lessons from the clinical cases of Fukuoka City Hospital, Department of Internal Medicine, Fukuoka, Japan].

More than 30% of the end stage liver cirrhosis was complicated by the impared glucose tolerance, in some of which insulin supplements may be required to control the blood glucose level. However, there are many unsolved issues on the cause and cares of hyperglycemia in cirrhotic men. Here, we presented a case of liver cirrhosis and hepatocellular caricnoma complicated by the severe glucose intolerance, and summarized our recent insulin therapy on the glucose intolerance of the decompensated liver cirrhosis in Fukuoka City Hospital, Department of Internal Medicine.

Carcinoma, Hepatocellular↗

PubMed1995

[Prevalence of diabetes mellitus and glucose intolerance in adult Ethiopian immigrants].

339 adult immigrants from Ethiopia were surveyed 1 year after arrival. They were screened for diabetes mellitus and impaired glucose tolerance by measurement of serum HgbA1C levels. The levels were higher than normal in 35 subjects (10.3%), and were significantly higher in immigrants consuming the Israeli diet, which is richer in proteins and carbohydrates, than in those on the Ethiopian diet. Oral glucose load was abnormal in 7 subjects. 3 had overt diabetes mellitus with absent serum insulin response to glucose load. 4 had glucose intolerance with normal insulin secretion. However, clinical appearance of diabetes was incidental and diabetes ketoacidosis was not detected. The overall prevalence of diabetes mellitus and glucose intolerance in this ethnic group (2.1%) is similar to that in the general population of Israel. Longitudinal studies would indicate the exact prevalence and type of diabetes mellitus among the Ethiopian immigrants.

Diabetes Mellitus↗

PubMed2004

Nerve conduction abnormalities in different stages of glucose intolerance.

AIMS: To look for changes in nerve conduction velocity (NCV) in early stages of glucose intolerance, i.e. in impaired glucose tolerance (IGT) and in asymptomatic newly diagnosed Type 2 diabetic subjects (NDD). MATERIALS AND METHODS: A total of 225 subjects were categorized as: Group 1: Subjects with normal glucose tolerance (NGT), Group 2: IGT subjects and Group 3: NDD subjects. Motor (MCV) and Sensory nerve Conduction Velocity (SCV) measurements were done. RESULTS: The mean MCV was significantly lower in the NDD group (47 +/- 5 m/s) when compared with the other two groups (IGT=50 +/-4.5 m/s; NGT= 53 +/- 4 m/s; P=0.0001). The IGT group of subjects also exhibited a significantly lower mean MCV when compared with the NGT subjects (P=0.0001). The mean SCV in the NDD group (42+10 m/s) was also significantly lower (P< 0.0007) than the NGT (46+6 m/s) and the IGT (48+10 m/s) groups. No significant difference in the mean SCV between the NGT and IGT groups was noted. In the multiple linear regression analysis both age and male gender were the risk factors for abnormal MCV and SCV. Abnormal MCV was found to be associated with 2-hr post glucose levels (R2 = 14.5%), while HbA1c (R2 = 4.9%) contributed towards abnormal SCV. CONCLUSION: Abnormal NCV is a common finding in NDD subjects. Slower mean MCV demonstrated by IGT subjects, calls for early screening of these subjects for complications.

Adult↗

PubMed2001

Glucose intolerance in obese adolescents with polycystic ovary syndrome: roles of insulin resistance and beta-cell dysfunction and risk of cardiovascular disease.

The roles of insulin resistance and insulin secretion in the pathogenesis of glucose intolerance in polycystic ovary syndrome (PCOS) were evaluated in 11 adolescents with impaired glucose tolerance (IGT) and 10 with normal glucose tolerance (NGT). Hepatic glucose production and insulin-stimulated glucose disposal were measured using [6,6-(2)H(2)]glucose and a 3-h hyperinsulinemic (80 mu/m(2).min)-euglycemic clamp. First and second phase insulin secretions were evaluated during a hyperglycemic clamp. Automated blood pressure measurements were made to assess the nocturnal change in blood pressure. Hepatic glucose production was significantly higher in IGT vs. NGT. Insulin-stimulated glucose disposal was not different between the two groups. The first phase insulin level was lower in IGT (207.9 +/- 21.0 vs. 357.0 +/- 62.9 muu/mL; P = 0.025; 1247 +/- 126 vs. 2142 +/- 377 pmol/L) without a difference in second phase insulin. The glucose disposition index (product of insulin sensitivity x first phase insulin) was lower in IGT vs. NGT (278 +/- 40 vs. 567 +/- 119 mg/kg.min; P = 0.023; 1546 +/- 223 vs. 3249 +/- 663 micromol/kg.min). The glucose disposition index correlated inversely with OGTT glucose concentrations at 30, 60, and 120 min. Adolescents with PCOS-IGT lacked the normal nocturnal decline in blood pressure. We conclude that in obese adolescents with PCOS, glucose intolerance is associated with 1) decreased first phase insulin secretion, 2) decreased glucose disposition index, and 3) increased hepatic glucose production. These metabolic abnormalities are precursors of type 2 diabetes and are present early in the course of PCOS. Furthermore, the absence of nocturnal dipping in blood pressure may herald the early expression of cardiovascular disease risk in these adolescents.

Adolescent↗

PubMedDate not supplied

Estimated prevalence of undiagnosed glucose intolerance from hyperandrogenic anovulation among women requesting electrolysis.

OBJECTIVE: Hyperandrogenic anovulation is the principal risk factor for non-insulin-dependent diabetes mellitus (NIDDM) in young women. Since many of these women undergo depilatory therapy, the purpose of this study was to estimate the probability of undiagnosed glucose intolerance associated with hyperandrogenic anovulation among premenopausal women requesting electrolysis. DESIGN: Case-series study. INTERVENTIONS: Women (N = 791) attending one of 27 electrology clinics in the United States, Canada and Germany received questionnaires requesting anthropometric data; personal information regarding age, surgery and medication use, and family histories of excess hair growth in female relatives and diabetes in parents or siblings. RESULTS: Of 652 respondents less than age 50 years, 643 (98.6%) women had hirsutism, of whom 465 had regular menstrual cycles. One hundred seventy-eight (27.3%) women less than 50 years of age had hirsutism with irregular menses, and one-half of these women also were obese. Regardless of adiposity, one-third of hirsute women with menstrual irregularity knew the cause of their androgen excess, while the remaining two-thirds were unaware of the reason for their excess hair growth. CONCLUSIONS: Assuming a 20% risk of glucose intolerance in obese hyperandrogenic anovulatory women by the fourth decade of life, the estimated prevalence of undiagnosed glucose intolerance from hyperandrogenic anovulation is 1.7% among women requesting electrolysis before age 50 years.

Adolescent↗

PubMed1982

Role of glucagon as a contributor to glucose intolerance in acute and chronic uremia.

It has been suggested that increased sensitivity to glucagon may contribute to glucose intolerance in uremia. In order to evaluate this possibility systematically, we have assessed the effect of glucagon on hepatic glucose outflow, formation of cAMP, and activation of adenylate cyclase by livers obtained from acutely and chronically uremic rats and their respective sham operated controls. Glucagon infused at rates of 6 ng/min/kg rat resulted in minimal and equivalent increases in hepatic glucose outflow and cAMP accumulation when livers from acutely uremic and control rats were perfused for 30 min. However, at glucagon infusion rates of 18 ng/min/kg, glucose efflux from perfused livers of acutely uremic rats was significantly reduced (p less than 0.001) compared to perfused livers of control rats (4.64 +/- .9 vs 12.7 +/- 2.4 mumol/g liver) and cAMP accumulation was also significantly lower (p less than 0.01) (1352 +/- 222 vs 3100 +/- 348 pmol/g liver). Basal adenylate cyclase activity of hepatic membranes obtained from uremic and control rats was similar, and was stimulated by glucagon concentrations ranging from 10(-8) to 10(-6) at equivalent rates in both groups. In livers from chronically uremic rats, glucagon infused at rates of 6 ng/kg/min significantly increased hepatic glucose outflow (32.5 +/- 6.9 mumol/g liver). However this was not greater than that of control animals (37.6 +/- 9.2). Furthermore, cAMP accumulation was significantly lower (p less than .02) in chronically uremic rats than in controls, and activation of adenylate cyclase by glucagon was similar in both groups. These findings indicate that glucagon does not increase glucose efflux, cAMP accumulation or enhance activation of adenylate cyclase by isolated perfused livers from either acutely or chronically uremic rats. Thus, glucose intolerance in uremic rats does not appear to be due to increase hepatic glucose output resulting from increased sensitivity to glucagon.

Acute Disease↗

PubMed2004

Glucose intolerance in a large cohort of mediterranean women with polycystic ovary syndrome: phenotype and associated factors.

The aim of this study was to investigate the phenotypic parameters and associated factors characterizing the development of glucose intolerance in polycystic ovary syndrome (PCOS). Among the 121 PCOS female subjects from the Mediterranean region, 15.7 and 2.5% displayed impaired glucose tolerance and type 2 diabetes, respectively. These subjects were included in a single group of overweight or obese subjects presenting with glucose intolerance (GI) states. PCOS women with normal glucose tolerance (81.8%) were subdivided into two groups: those who were overweight or obese and those of normal weight. Metabolic and hormonal characteristics of the GI group included significantly higher fasting and glucose-stimulated insulin levels, more severe insulin resistance, hyperandrogenemia, and significantly higher cortisol and androstenedione responses to 1-24 ACTH stimulation. One important finding was that lower birth weight and earlier age of menarche were associated with GI in PCOS women. Frequency of hirsutism, oligomenorrhea, acne, and acanthosis nigricans did not characterize women with GI. Our findings indicate that PCOS patients with GI represent a subgroup with specific clinical and hormonal characteristics. Our observations may have an important impact in preventative and therapeutic strategies.

Adolescent↗

PubMed1977

Fetal pancreatic glucagon responses in glucose-intolerant nonhuman primate pregnancy.

Rhesus monkey pancreatic alpha-cell function in streptozotoc-induced glucose-intolerant pregnancy is similar to that in normal primate pregnancy. Specifically, basal maternal and fetal plasma glucagon levels equate, and the fetal alpha cell does not respond to the glucagonogenic stimulus of either intravenous alanine or insulin-induced hypoglycemia. This contrasts with the accelerated maturation of the fetal beta cell in glucose-intolerant pregnancy, and does not support the concept of functional coupling of the pancreatic islet by a common glucose-based process. Fetal plasma glucagon levels do increase after L-dopa injection to the fetus. These data indicate that alpha cell unresponsiveness is a function of the glucagon-releasing mechanism rather than inadequate hormonal synthesis.

Alanine↗

PubMed1997

Gestational diabetes mellitus and glucose intolerance in a Mexican population.

OBJECTIVE: To determine the prevalence of gestational diabetes mellitus (GDM), glucose intolerance (GI) and macrosomia in a Latin Mexican population, using the one-step procedure proposed by the World Health Organization. METHOD: Consecutive pregnant women (n = 667) who attended the antenatal clinic and delivered at the hospital were recruited after 24 weeks of gestation, mean 34.2 weeks, range 24-40 weeks. After a minimum of 3 days with a 150-g carbohydrate diet, a glucose load of 75 g was administered and 2 h after, a blood sample for glucose was taken, plasma was separated and immediately processed for glucose, using a glucose-oxidase method. RESULTS: Twenty women were diagnosed with GDM (3%), 87 had GI (13%) and 560 had a normal glucose response (84%). Macrosomia occurred in two (10%) of GDM, in nine (10.3%) of GI, and in 29 (5.4%) gravidas with a normal response, respectively. Only one of the macrosomic infants whose mother had GI, had neonatal hypoglycemia and hyperbilirubinemia. CONCLUSION: The overall prevalence of glucose abnormalities during pregnancy was 16%. GI in this group was associated to macrosomia at the same rate as GDM.

Adult↗

PubMed2006

Calcium channel blocker azelnidipine reduces glucose intolerance in diabetic mice via different mechanism than angiotensin receptor blocker olmesartan.

The potential combined effect and mechanism of calcium channel blockers (CCB) and angiotensin II type 1 receptor blockers (ARB) to improve insulin resistance were investigated in type 2 diabetic KK-Ay mice, focusing on their antioxidative action. Treatment of KK-Ay mice with a CCB, azelnidipine (3 mg/kg/day), or with an ARB, olmesartan (3 mg/kg/day), for 2 weeks lowered the plasma concentrations of glucose and insulin in the fed state, attenuated the increase in plasma glucose in the oral glucose tolerance test (OGTT), and increased 2-[(3)H]deoxy-d-glucose (2-[(3)H]DG) uptake into skeletal muscle with the increase in translocation of glucose transporter 4 (GLUT4) to the plasma membrane. Both blockers also decreased the in situ superoxide production in skeletal muscle. The decrease in plasma concentrations of glucose and insulin in the fed state and superoxide production in skeletal muscle, as well as GLUT4 translocation to the plasma membrane, after azelnidipine administration was not significantly affected by coadministration of an antioxidant, 2,2,6,6-tetramethyl-1-piperidinyloxy (tempol). However, those changes caused by olmesartan were further improved by tempol. Moreover, olmesartan enhanced the insulin-induced tyrosine phosphorylation of insulin receptor substrate-1 induced in skeletal muscle, whereas azelnidipine did not change it. Coadministration of azelnidipine and olmesartan further decreased the plasma concentrations of glucose and insulin, improved OGTT, and increased 2-[(3)H]DG uptake in skeletal muscle. These results suggest that azelnidipine improved glucose intolerance mainly through inhibition of oxidative stress and enhanced the inhibitory effects of olmesartan on glucose intolerance, as well as the clinical possibility that the combination of CCB and ARB could be more effective than monotherapy in the treatment of insulin resistance.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2002

Size at birth and glucose intolerance in a relatively genetically homogeneous, high-birth weight population.

BACKGROUND: The results of epidemiologic studies have linked birth size to adult glucose intolerance. OBJECTIVE: We investigated this association in a genetically homogeneous population with higher birth weights and a lower prevalence of type 2 diabetes than previously studied. DESIGN: The subjects were 2362 men and 2286 women aged 33-65 y. Size at birth was obtained from the National Archives of Iceland. Data for adult anthropometry, fasting blood glucose, and blood glucose after an oral glucose load came from the randomized prospective Reykjavík Study. RESULTS: Postchallenge glucose concentrations were inversely related to birth weight and length in men and inversely related to birth weight and ponderal index in women (P < 0.001). This association was mainly found among those within the highest one-third of adult body mass index values. In men, the prevalence of dysglycemia was lower with increasing weight (P = 0.04) and length (P = 0.003) at birth but there was no relation of dysglycemia to ponderal index. For women, there was no linear trend for dysglycemia in relation to size at birth but the relation with birth length was U shaped. CONCLUSIONS: Greater birth weight and length appear to offer a protective effect against glucose intolerance. Adult overweight or obesity enhances the risk associated with low birth weight and length. Because the population studied has higher birth weights and a lower prevalence of type 2 diabetes than are found in neighboring countries, it is possible that decreasing the number of low-birth weight infants might help to stem the increasing prevalence of type 2 diabetes worldwide.

Adult↗

PubMed1997

Effect of overweight and obesity on glucose intolerance and dyslipidemia in Saudi Arabia, epidemiological study.

The aim of this study was to study the effect of overweight and obesity on glucose intolerance and dyslipidemia in Saudi Arabia. A cross-sectional national epidemiological randomized household survey of 2059 Saudi subjects, aged 30-64 years was carried out. The sample was representative and was in accordance with the national population distribution with respect to age, gender, regional and residency, urban versus rural population distribution. The subjects height and weight for the calculation of body mass index (BMI) was measured. Blood samples were drawn and assayed for glucose, total cholesterol, triglyceride and high density lipoprotein (HDL). Low density lipoprotein (LDL) was calculated. The oral glucose tolerance test was carried out for subjects with borderline random glucose concentration and the overall prevalence of diabetes mellitus was calculated. A high prevalence of obesity among the Saudi population was observed and mean serum glucose concentration was significantly higher among overweight and obese groups. The prevalence of diabetes mellitus was significantly higher among obese groups. The mean serum triglyceride concentration was only significantly higher among male obese groups. There was no significant difference in the mean of serum total cholesterol concentration between control and obese groups. Mean serum HDL concentration was lower among the obese group, however, the difference was not significant. There was no significant difference in the prevalence of hypercholesterolemia between control and obese groups. Prevalence of hypertriglyceridemia was higher among obese groups and was significantly higher among male subjects across all BMI groups. Prevalence of hypo HDL cholesterolemia exceeded 50% of the study population. Obesity, glucose intolerance, hypertriglyceridemia, hypo HDL cholesterolemia and features of insulin resistance syndrome (IRS) are widely prevalent among the Saudi population over the age of 40 years. IRS is probable a significant contributor to the pathologic process of cardiovascular (CVD) disease among the Saudi population, especially in view of the low prevalence of hypercholesterolemia.

Adult↗

PubMed1998

Weight history, glucose intolerance, and insulin levels in middle-aged Swedish men.

The association between weight history and glucose intolerance was examined in a cross-sectional study consisting of 3,128 Swedish men aged 35-56 years, 52 percent of whom had a family background of diabetes mellitus. Oral glucose tolerance testing detected 55 cases of type 2 (non-insulin-dependent) diabetes and 172 cases of impaired glucose tolerance. Among men with no family history of diabetes, the estimated odds ratios for impaired glucose tolerance associated with short (<5 years) and long (> or =10 years) durations of obesity (body mass index (weight (kg)/height2 (m2) > or =25.0) were 1.3 (95% confidence interval (CI) 0.2-7.7) and 11.8 (95% CI 3.3-41.9), respectively. Among men with a family history of diabetes, the odds ratios were 2.0 (95% CI 0.8-4.7) and 4.0 (95% CI 1.8-9.1), respectively. Corresponding estimates of the odds of type 2 diabetes, adjusted for family history of diabetes, were 1.9 (95% CI 0.5-7.1) and 7.3 (95% CI 2.2-23.7), respectively. The odds of high (> or =30.0 mU/liter) fasting insulin levels in subjects with impaired glucose tolerance were 6.9 (95% CI 0.6-74.2) and 21.0 (95% CI 2.1-206.4) for short and long durations of obesity, respectively. Corresponding estimated odds of low 2-hour insulin response (< or =71.9 mU/liter) were 0.7 (95% CI 0.2-2.9) and 3.3 (95% CI 1.2-8.9). Homeostasis model assessment of insulin resistance yielded an odds ratio of 6.7 (95% CI 0.6-73.4) for a short duration of obesity and 20.0 (95% CI 2.0-200.6) for a long duration. Examination of beta-cell function with homeostasis model assessment resulted in odds ratios of 0.2 (95% CI 0.0-1.6) and 2.0 (95% CI 0.7-5.4) for short and long durations of obesity, respectively. These data indicate that obesity decreases glucose tolerance by way of progressively increased insulin resistance and, in the case of prolonged duration, by decreased insulin secretion as well.

Body Mass Index↗

PubMed1975

Glucose intolerance in the carcinoid syndrome.

We assayed glucose tolerance and insulin secretion in ten patients with metastatic carcinoid tumors and the carcinoid syndrome ("active tumors") and in seven patients with metastatic carcinoid tumors without the carcinoid syndrome ("inactive tumors"). The patients with "active tumors" had elevated serum serotonin levels while the patients with "inactive tumors" had normal serum serotonin levels. Of the ten patients with "active tumors," five had diabetic and three had borderline intravenous glucose disposal rate constants (KG = 0.88 +/- 0.07, M. +/- S.E.M.). Their KG was significantly lower (p less than 0.01) than a group of age-matched normals. All of the patients with "inactive tumors" had normal KG values (KG = 1.67 +/- 0.24). Their KG did not differ from that of age-matched normal subjects. Both groups of carcinoid patients had a comparable decrease in their insulinogenic index. Two days' administration of the serotonin antagonist cyproheptadine (Cypro) to eight of the patients with "active tumors" resulted in a significant increase in the "insulinogenic index" (50%) but a nonsignificant increase in the KG (12%). Administration of p-chlorophenylalanine, a compound that blocks serotonin synthesis, resulted in an increase in both the KG (60%) and the "insulinogenic index" (55%). The insulin half-life (t1/2) of patients with "active tumors" (6.1 +/- 0.4 min.) did not differ from the t1/2 of normal subjects (6.6 +/- 0.4 min.), suggesting that the decreased plasma insulin levels following intravenous glucose were due to impaired insulin secretion rather than accelerated insulin destruction. Seven of the patients received treatment with the antitumor agent streptozotocin (Strepto). The patients received cumulative doses of from 70 to 300 mg. of Strepto per kilogram body weight with no impairment in glucose tolerance or insulin secretion. We conclude that there is high incidence of glucose intolerance (80%) and impaired insulin secretion in patients with the carcinoid syndrome and that serotonin plays a role in producing these alterations.

Adult↗