scholarly journals Low-density lipoprotein cholesterol is associated with insulin secretion

2021 ◽  
Author(s):  
Corinna Dannecker ◽  
Robert Wagner ◽  
Andreas Peter ◽  
Julia Hummel ◽  
Andreas Vosseler ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Ldl Cholesterol ◽  
Density Lipoprotein ◽  
Insulin Clearance ◽  
Oral Glucose ◽  
Insulinogenic Index ◽  
Glucose Load ◽  
Cholesterol Lowering ◽  
C Peptide ◽  
Increased Risk

Abstract Objective Pharmacological lowering of LDL cholesterol potently reduces cardiovascular risk while concurrently increasing type 2 diabetes risk. The aim of this study was to investigate the relationship between LDL cholesterol concentrations and insulin secretion and glucagon levels. Methods 3,039 subjects without cholesterol lowering therapy, but with increased risk for diabetes, underwent routine blood tests and a 5-point oral glucose tolerance test (OGTT). Glucagon concentrations, insulin secretion and insulin clearance indices were derived from the OGTT. Results There was no association between LDL cholesterol and fasting glucagon (p=0.7, ß=-0.01) or post glucose load glucagon levels (p=0.7, ß=-0.07), but we detected significant positive associations of LDL cholesterol and C-peptide-based indices of insulin secretion (AUCC-Peptide(0-30min)/AUCGlucose(0-30min): p=0.0001, ß=0.06; AUCC-Peptide(0-120min)/AUCGlucose(0-120min): p<0.0001, ß=-0.08). In contrast we found a negative association of insulin-based insulin secretion indices with LDL concentrations (Insulinogenic index: p=0.014, ß=-0.04; disposition index: p=0.0005, ß=-0.06). Though, LDL cholesterol levels were positively associated with insulin clearance assessed from C-peptide and insulin concentrations, both in the fasting state and post glucose load (p<0.0001, ß=0.09 and p<0.0001, ß=0.06, respectively). Conclusion As C-peptide based indices reflect insulin secretion independent of hepatic clearance, our results indicate lower insulin secretion in case of lesser LDL cholesterol. This could explain deteriorating glycemic control in response to cholesterol lowering drugs.

scholarly journals Fasting insulin reflects heterogeneous physiological processes: role of insulin clearance

2011 ◽  
Vol 301 (2) ◽  
pp. E402-E408 ◽  
Author(s):  
Mark O. Goodarzi ◽  
Jinrui Cui ◽  
Yii-Der I. Chen ◽  
Willa A. Hsueh ◽  
Xiuqing Guo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Waist Circumference ◽  
Mexican Americans ◽  
Fasting Glucose ◽  
Insulin Clearance ◽  
Oral Glucose ◽  
Metabolic Clearance ◽  
Insulinogenic Index ◽  
Fasting Insulin

Several processes contribute to variation in fasting insulin concentration, including fasting glucose, insulin resistance, insulin secretion, and insulin clearance. Our goal was to determine the relative contribution of each of these insulin-related traits, plus anthropometric parameters, to fasting insulin among 470 Mexican Americans. The euglycemic hyperinsulinemic clamp yielded insulin sensitivity (M value) and metabolic clearance rate of insulin (MCRI). Acute insulin secretion was estimated by the insulinogenic index (IGI30) from the oral glucose tolerance test. Regression (univariate) and generalized estimating equations (multivariate) were used to describe the relationship of insulin-related traits to fasting insulin. Univarate analyses were used to select which traits to include in the multivariate model. In multivariate analysis, MCRI, M, BMI, waist circumference, and fasting glucose were independently associated with fasting insulin. Decreasing M and MCRI were associated with increasing fasting insulin, whereas increasing BMI, waist circumference, and fasting glucose were associated with increasing fasting insulin. Standardized coefficients allowed determination of the relative strength of each trait's association with fasting insulin in the entire cohort (strongest to weakest): MCRI (−0.35, P < 0.0001), M (−0.24, P < 0.0001), BMI (0.20, P = 0.0011), waist circumference (0.16, P = 0.021), and fasting glucose (0.11, P = 0.014). Fasting insulin is a complex phenotype influenced by several independent processes, each of which might have its own environmental and genetic determinants. One of the most associated traits was insulin clearance, which has implications for studies that have used fasting insulin as a surrogate for insulin resistance.

scholarly journals Relationship between Insulin Secretion and Arterial Stiffness in Essential Hypertension

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Yancui Sun ◽  
Yanqiu Zhu ◽  
Lu Zhang ◽  
Yan Lu ◽  
Yan Liu ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Arterial Stiffness ◽  
Glucose Tolerance ◽  
Linear Regression Analysis ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Oral Glucose ◽  
C Peptide ◽  
Hypertensive Patients

The study aims to explore the relationship between plasma insulin secretion and arterial stiffness in nondiabetic essential hypertensive patients. A total of 730 nondiabetic essential hypertensive patients registered between January 2016 and October 2020 were enrolled. A two-hour oral glucose tolerance test (OGTT) was performed to detect the levels of C-peptide and blood glucose at 0 hours and 2 hours, as well as the difference between C-peptide (Δ C-peptide) and blood glucose (Δ blood glucose) over the same period. Patients were divided into two groups: the normal glucose tolerance (NGT) group (n = 322) and the impaired glucose tolerance (IGT) group (n = 408). A multiple linear regression analysis was used to evaluate the association between brachial-ankle pulse wave velocity (baPWV) and the other factors. 0 h C-peptide, 2 h C-peptide, and Δ C-peptide were found to be higher in the IGT group. baPWV was positively linear correlated with 2 h C-peptide (r = 0.086, p = 0.020 ) and Δ C-peptide (r = 0.115, p = 0.002 ). baPWV remained independently associated with 0 h C-peptide, 2 h C-peptide, and Δ C-peptide, after adjusting by age, gender, smoking, body mass index (BMI), high-density lipoprotein (HDL), cholesterol, systolic blood pressure (SBP), and triglycerides (TG). Our data shows that higher endogenous insulin secretion might play an important role in the progression of arterial stiffness in nondiabetic essential hypertensive patients.

Nighttime snacking reduces whole body fat oxidation and increases LDL cholesterol in healthy young women

2013 ◽  
Vol 304 (2) ◽  
pp. R94-R101 ◽  
Author(s):  
Masanobu Hibi ◽  
Ayumi Masumoto ◽  
Yuri Naito ◽  
Kahori Kiuchi ◽  
Yayoi Yoshimoto ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Fat Oxidation ◽  
Tolerance Test ◽  
Whole Body ◽  
Oral Glucose ◽  
Night Time ◽  
Snack Consumption

The increase in obesity and lipid disorders in industrialized countries may be due to irregular eating patterns. Few studies have investigated the effects of nighttime snacking on energy metabolism. We examined the effects of nighttime snacking for 13 days on energy metabolism. Eleven healthy women (means ± SD; age: 23 ± 1 yr; body mass index: 20.6 ± 2.6 kg/m2) participated in this randomized crossover trial for a 13-day intervention period. Subjects consumed a specified snack (192.4 ± 18.3 kcal) either during the daytime (10:00) or the night time (23:00) for 13 days. On day 14, energy metabolism was measured in a respiratory chamber without snack consumption. An oral glucose tolerance test was performed on day 15. Relative to daytime snacking, nighttime snacking significantly decreased fat oxidation (daytime snacking: 52.0 ± 13.6 g/day; nighttime snacking: 45.8 ± 14.0 g/day; P = 0.02) and tended to increase the respiratory quotient (daytime snacking: 0.878 ± 0.022; nighttime snacking: 0.888 ± 0.021; P = 0.09). The frequency of snack intake and energy intake, body weight, and energy expenditure were not affected. Total and low-density lipoprotein (LDL) cholesterol significantly increased after nighttime snacking (152 ± 26 mg/dl and 161 ± 29 mg/dl; P = 0.03 and 76 ± 20 mg/dl and 83 ± 24 mg/dl; P = 0.01, respectively), but glucose and insulin levels after the glucose load were not affected. Nighttime snacking increased total and LDL cholesterol and reduced fat oxidation, suggesting that eating at night changes fat metabolism and increases the risk of obesity.

scholarly journals Experimental BPA Exposure and Glucose-Stimulated Insulin Response in Adult Men and Women

2018 ◽  
Vol 2 (10) ◽  
pp. 1173-1187 ◽  
Author(s):  
Richard W Stahlhut ◽  
John Peterson Myers ◽  
Julia A Taylor ◽  
Angel Nadal ◽  
Jonathan A Dyer ◽  
...  
Keyword(s):  
Environmental Protection Agency ◽  
Metabolic Diseases ◽  
Insulin Response ◽  
Percentage Change ◽  
Oral Glucose ◽  
Insulinogenic Index ◽  
Strong Positive Correlation ◽  
Control Session ◽  
Cross Sectional ◽  
C Peptide

Abstract Context Human cross-sectional and animal studies have shown an association of the chemical bisphenol A (BPA) with insulin resistance, type 2 diabetes, and other metabolic diseases, but no human experimental study has investigated whether BPA alters insulin/C-peptide secretion. Design Men and postmenopausal women (without diabetes) were orally administered either the vehicle or a BPA dose of 50 µg/kg body weight, which has been predicted by US regulators (Food and Drug Administration, Environmental Protection Agency) to be the maximum, safe daily oral BPA dose over the lifetime. Insulin response was assessed in two cross-over experiments using an oral glucose tolerance test (OGTT; experiment 1) and a hyperglycemic (HG) clamp (experiment 2). Main outcomes were the percentage change of BPA session measures relative to those of the control session. Results Serum bioactive BPA after experimental exposure was at levels detected in human biomonitoring studies. In the OGTT, a strong positive correlation was found between hemoglobin A1c(HbA1c) and the percentage change in the insulinogenic index (Spearman = 0.92), an indicator of early-phase insulin response, and the equivalent C-peptide index (Pearson = 0.97). In the HG clamp study, focusing on the later-phase insulin response to a stable level of glucose, several measures of insulin and C-peptide appeared suppressed during the BPA session relative to the control session; the change in insulin maximum concentration (Cmax) was negatively correlated with HbA1c and the Cmax of bioactive serum BPA. Conclusions This exploratory study suggests that BPA exposure to a dose considered safe by US regulators may alter glucose-stimulated insulin response in humans.

Elevated apolipoprotein A1 and HDL cholesterol associated with age-related macular degeneration: two population cohorts

2021 ◽  
Author(s):  
Liv Tybjærg Nordestgaard ◽  
Anne Tybjærg-Hansen ◽  
Ruth Frikke-Schmidt ◽  
Børge Grønne Nordestgaard
Keyword(s):  
Macular Degeneration ◽  
Ldl Cholesterol ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Age Related Macular Degeneration ◽  
Apolipoprotein A1 ◽  
Age Related ◽  
Hazard Ratios ◽  
Increased Risk ◽  
Plasma Apolipoprotein

Abstract Context To enable prevention and treatment of age-related macular degeneration(AMD), understanding risk factors for AMD is important. Objective We tested the hypotheses that elevated plasma apolipoprotein A1 and high-density lipoprotein(HDL) cholesterol, and low levels of low-density lipoprotein(LDL) cholesterol, are associated with increased risk of AMD. Design and Setting From the Danish general population, we studied 106,703 and 16,032 individuals in the Copenhagen General Population Study(CGPS) and the Copenhagen City Heart Study(CCHS) with median follow-up of respectively 9 and 32 years. Main Outcome Measures 1,787 AMD in CGPS and 206 in CCHS. Results Higher concentrations of plasma apolipoprotein A1 and HDL cholesterol, and lower concentrations of LDL cholesterol, were associated with higher risk of AMD in CGPS. After multifactorial adjustment, individuals in the highest versus lowest quartile of plasma apolipoprotein A1 and HDL cholesterol had hazard ratios for AMD of 1.40(95%CI:1.20-1.63) and 1.22(1.03-1.45). Corresponding hazard ratios for individuals in the lowest versus highest quartile of LDL cholesterol were 1.18(1.02-1.37). Per 100 mg/dL higher plasma apolipoprotein A1, 1 mmol/L(39 mg/dL) higher HDL, and 1 mmol/L(39mmol/L) lower LDL cholesterol, the hazard ratios for AMD were 1.53(1.31-1.80), 1.19(1.07-1.32), and 1.05(1.00-1.11), respectively, with similar results across strata of different risk factors. Higher concentrations of HDL cholesterol were also associated with higher risk of AMD in the CCHS. Conclusion Elevated plasma apolipoprotein A1 and HDL cholesterol, and lower LDL cholesterol, are associated with increased risk of age-related macular degeneration.

scholarly journals Hypoglycemia and Islet Dysfunction Following Oral Glucose Tolerance Testing in Pancreatic-Insufficient Cystic Fibrosis

2020 ◽  
Vol 105 (10) ◽  
pp. 3179-3189
Author(s):  
Marissa J Kilberg ◽  
Clea Harris ◽  
Saba Sheikh ◽  
Darko Stefanovski ◽  
Marina Cuchel ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Early Phase ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Insulin Effect ◽  
Secretory Rate ◽  
C Peptide ◽  
Islet Dysfunction

Abstract Context Oral glucose tolerance test (OGTT)-related hypoglycemia is common in pancreatic-insufficient cystic fibrosis (PI-CF), but its mechanistic underpinnings are yet to be established. Objective To delineate the mechanism(s) underlying OGTT-related hypoglycemia. Design and Setting We performed 180-minute OGTTs with frequent blood sampling in adolescents and young adults with PI-CF and compared results with those from a historical healthy control group. Hypoglycemia (Hypo[+]) was defined as plasma glucose &lt;65 mg/dL. We hypothesized that CF-Hypo[+] would demonstrate impaired early phase insulin secretion and persistent late insulin effect compared with control-Hypo[+], and explored the contextual counterregulatory response. Main Outcome Measure OGTT 1-hour and nadir glucose, insulin, C-peptide, and insulin secretory rate (ISR) incremental areas under the curve (AUC) between 0 and 30 minutes (early) and between 120 and 180 minutes (late), and Δglucagon120-180min and Δfree fatty acids (FFAs)120-180min were compared between individuals with CF and control participants with Hypo[+]. Results Hypoglycemia occurred in 15/23 (65%) patients with CF (43% female, aged 24.8 [14.6-30.6] years) and 8/15 (55%) control participants (33% female, aged 26 [21-38] years). The CF-Hypo[+] group versus the control-Hypo[+] group had higher 1-hour glucose (197 ± 49 vs 139 ± 53 mg/dL; P = 0.05) and lower nadir glucose levels (48 ± 7 vs 59 ± 4 mg/dL; P &lt; 0.01), while insulin, C-peptide, and ISR-AUC0-30 min results were lower and insulin and C-peptide, and AUC120-180min results were higher (P &lt; 0.05). Individuals with CF-Hypo[+] had lower Δglucagon120-180min and ΔFFA120-180min compared with the control-Hypo[+] group (P &lt; 0.01). Conclusions OGTT-related hypoglycemia in PI-CF is associated with elevated 1-hour glucose, impaired early phase insulin secretion, higher late insulin exposure, and less increase in glucagon and FFAs. These data suggest that hypoglycemia in CF is a manifestation of islet dysfunction including an impaired counterregulatory response.

Effects of acute α2-blockade on insulin action and secretion in humans

1998 ◽  
Vol 274 (1) ◽  
pp. E57-E64 ◽  
Author(s):  
Andrea Natali ◽  
Amalia Gastaldelli ◽  
Alfredo Quiñones Galvan ◽  
Anna Maria Sironi ◽  
Demetrio Ciociaro ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Energy Expenditure ◽  
Plasma Insulin ◽  
Time Course ◽  
Resting Energy Expenditure ◽  
Oral Glucose ◽  
Cardiac Work ◽  
C Peptide ◽  
Glucose Ingestion ◽  
Resting Energy

We tested whether acute α2-blockade affects insulin secretion, glucose and fat metabolism, thermogenesis, and hemodynamics in humans. During a 5-h epinephrine infusion (50 ng ⋅ min−1 ⋅ kg−1) in five volunteers, deriglidole, a selective α2-receptor inhibitor, led to a more sustained rise in plasma insulin and C-peptide levels (+59 ± 14 vs. +28 ± 6, and +273 ± 18 vs. +53 ± 14 pM, P < 0.01 vs. placebo) despite a smaller rise in plasma glucose (+0.90 ± 0.4 vs. +1.5 ± 0.3 mM, P < 0.01). Another 10 subjects were studied in the postabsorptive state and during a 4-h hyperglycemic (+4 mM) clamp, coupled with the ingestion of 75 g of glucose at 2 h. In the postabsorptive state, hepatic glucose production, resting energy expenditure, and plasma insulin, free fatty acid (FFA), and potassium concentrations were not affected by acute α2-blockade. Hyperglycemia elicited a biphasic rise in plasma insulin (to a peak of 140 ± 24 pM), C-peptide levels (1,520 ± 344 pM), and insulin secretion (to 410 ± 22 pmol/min); superimposed glucose ingestion elicited a further twofold rise in insulin and C-peptide levels, and insulin secretion. However, α2-blockade failed to change these secretory responses. Fasting blood β-hydroxybutyrate and glycerol and plasma FFA and potassium concentrations all declined with hyperglycemia; time course and extent of these changes were not affected by α2-blockade. Resting energy expenditure (+25 vs. +16%, P < 0.01) and external cardiac work (+28% vs. +19%, P < 0.01) showed larger increments after α2-blockade. We conclude that acute α2-blockade in humans 1) prevents epinephrine-induced inhibition of insulin secretion, 2) does not potentiate basal or intravenous- or oral glucose-induced insulin release, 3) enhances thermogenesis, and 4) increases cardiac work.

scholarly journals The relationship between fasting hyperglycemia and insulin secretion in subjects with normal or impaired glucose tolerance

2008 ◽  
Vol 295 (2) ◽  
pp. E401-E406 ◽  
Author(s):  
Muhammad A. Abdul-Ghani ◽  
Masafumi Matsuda ◽  
Rucha Jani ◽  
Christopher P. Jenkinson ◽  
Dawn K. Coletta ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Plasma Glucose ◽  
Early Phase ◽  
Mexican Americans ◽  
Late Phase ◽  
Oral Glucose ◽  
C Peptide ◽  
The Relationship

To assess the relationship between the fasting plasma glucose (FPG) concentration and insulin secretion in normal glucose tolerance (NGT) and impaired glucose tolerance (IGT) subjects, 531 nondiabetic subjects with NGT ( n = 293) and IGT ( n = 238; 310 Japanese and 232 Mexican Americans) received an oral glucose tolerance test (OGTT) with measurement of plasma glucose, insulin, and C-peptide every 30 min. The insulin secretion rate was determined by plasma C-peptide deconvolution. Insulin sensitivity (Matsuda index) was measured from plasma insulin and glucose concentrations. The insulin secretion/insulin resistance (IS/IR) or disposition index was calculated as ΔISR/ΔG ÷ IR. As FPG increased in NGT subjects, the IS/IR index declined exponentially over the range of FPG from 70 to 125 mg/dl. The relationship between the IS/IR index and FPG was best fit with the equation: 28.8 exp(−0.036 FPG). For every 28 mg/dl increase in FPG, the IS/IR index declined by 63%. A similar relationship between IS/IR index and FPG was observed in IGT. However, the decay constant was lower than in NGT. The IS/IR index for early-phase insulin secretion (0–30 min) was correlated with the increase in FPG in both NGT and IGT ( r = −0.43, P < 0.0001 and r = −0.20, P = 0.001, respectively). However, the correlation between late-phase insulin secretion (60–120 min) and FPG was not significant. In conclusion, small increments in FPG, within the “normal” range, are associated with a marked decline in glucose-stimulated insulin secretion and the decrease in insulin secretion with increasing FPG is greater in subjects with NGT than IGT and primarily is due to a decline in early-phase insulin secretion.

Twenty-four hour C-peptide and insulin secretion rates and diurnal profiles of glucose, lipids and intermediary metabolites in cirrhosis

1992 ◽  
Vol 83 (5) ◽  
pp. 597-605 ◽  
Author(s):  
Yolanta T. Kruszynska ◽  
Janet Munro ◽  
Philip D. Home ◽  
Neil McIntyre
Keyword(s):  
Insulin Secretion ◽  
Fatty Acid ◽  
Serum Insulin ◽  
Insulin Clearance ◽  
Metabolic Clearance ◽  
Intermediary Metabolites ◽  
C Peptide ◽  
Control Subjects ◽  
Glucose Profiles ◽  
Cirrhotic Patients

1. To examine the contributions of hypersecretion and decreased insulin clearance to the hyperinsulinaemia of cirrhosis, insulin secretion was calculated over the day from serum C-peptide concentrations and C-peptide metabolic clearance rate. The latter was measured during infusions of recombinant human C-peptide. In cirrhotic patients (n = 9) insulin secretion rate was twice that of normal control subjects (n = 10), both in the basal state [02.00–07.00 hours, 15.7 ± 2.1 (mean ± sem) nmol/h (2.6 ± 0.4 units/h) versus 7.0 ± 0.9 nmol/h (1.2 ± 0.2 units/h), P<0.002] and over 24 h [787 ± 93 nmol (132 ± 16 units) versus 346 ± 34 nmol (58 ± 6 units), P<0.001]. However, the area under the serum insulin concentration curve was approximately six times greater in the cirrhotic patients (24 h basal, 6.3 ± 1.0 versus 1.1 ± 0.31 nmol l−1 h, P<0.001; 24 h total, 21.7 ± 3.2 versus 3.7 ± 0.7 nmol l−1 h, P<0.001). Thus, despite impairment of insulin clearance there is continuing hyper-section of insulin in cirrhosis. 2. The relationship of carbohydrate and lipid metabolism with insulin secretion was assessed. In cirrhotic patients, 24 h blood glucose profiles showed a worsening of glucose tolerance over breakfast, despite greater insulin secretion compared with other meals, suggesting that the insulin insensitivity of cirrhosis is worse at this time. 3. Cirrhotic patients showed impaired suppression of blood glycerol levels after meals but normal suppression of serum non-esterified fatty acid concentrations. The greatest differences in the profiles of serum lipids and lipid-related metabolites in cirrhotic patients and control subjects occurred at night. Whereas in control subjects, serum non-esterified fatty acid, blood glycerol and blood 3-hydroxybutyrate concentrations peaked between 01.00 and 03.00 hours, falling gradually thereafter until 08.00 hours, in cirrhotic patients serum non-esterified fatty acid and blood glycerol levels showed a gradual increase during the night to reach maximal levels at 08.00 hours when they were twice those of control subjects (P<0.001). 4. The blood 3-hydroxybutyrate and serum triacyl-glycerol profiles suggested that in cirrhotic patients there was preferential utilization of non-esterified fatty acids for ketogenesis and reduced re-esterification to triacylglycerol.

Glucose intolerance in thyrotoxicosis roles of insulin, glucagon and somatostatin

1987 ◽  
Vol 114 (2) ◽  
pp. 228-234 ◽  
Author(s):  
Karen S. L. Lam ◽  
Rose T. T. Yeung ◽  
Patricia W. M. Ho ◽  
S. K. Lam
Keyword(s):  
B Cell ◽  
Glucose Intolerance ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Oral Glucose ◽  
Insulinogenic Index ◽  
C Peptide ◽  
Pancreatic B Cell ◽  
Significant Difference ◽  
Glucose Ingestion

Abstract. The responses in plasma glucose, insulin, C-peptide, glucagon and somatostatin to an oral glucose load were studied in 10 thyrotoxic patients and 10 matched euthyroid controls. The thyrotoxic patients had higher mean fasting plasma glucose (P < 0.05) and responded to oral glucose with an earlier peak at 30 min which was higher than the corresponding glucose level in the controls (P < 0.05). Impaired glucose tolerance was found in 3 patients. Fasting insulin and C-peptide levels were normal in the thyrotoxic patients when corrected for the higher glucose levels. Following glucose ingestion, there was no significant difference between the areas under the insulin or C-peptide curves in patients and controls, but Seltzer's insulinogenic index was reduced in the patients (P < 0.01) suggesting an impaired pancreatic B-cell response to oral glucose. Mean basal glucagon was normal in the thyrotoxic patients. However, while in the controls plasma glucagon became suppressed following glucose ingestion (P < 0.0001), no significant suppression was found in the patients. In the thyrotoxic patients, mean basal somatostatin was normal, but the area under the somatostatin curve following glucose ingestion was significantly increased (P < 0.02). Our findings suggest that décreased glucagon suppression and impaired insulin response after glucose ingestion are involved in glucose intolerance in thyrotoxicosis. Enhanced somatostatin responses to oral glucose in thyrotoxicosis may have contributed to the observed impairment in pancreatic B-cell responsiveness.

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