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Results for “Glucose Intolerance”

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PubMed1998

Glucose intolerance in familial combined hyperlipidaemia. EUFAM study group.

BACKGROUND: Familial combined hyperlipidaemia (FCHL) is a common hereditary disorder. Hypertriglyceridaemia is associated with glucose intolerance and insulin resistance. METHODS: To study glucose tolerance in FCHL patients with different lipid phenotypes [hypercholesterolaemia (IIA), mixed hyperlipidaemia (IIB), hypertriglyceridaemia (IV)], we investigated 253 family members and 92 spouses arising from 33 well-defined Finnish FCHL pedigrees. RESULTS: In oral glucose tolerance tests the affected family members had higher values for glucose area under the curve than did non-affected family members [673+/-127 min mmolL(-1), 754+/-145 min mmol L(-1), 846+/-180 min mmol L(-1) and 838+/-183 min mmol L(-1) for phenotypes normal, IIA, IIB and IV respectively; P < 0.001 after adjustment for body mass index, waist circumference and age]. Impaired glucose tolerance and diabetes were more common among affected than non-affected family members (prevalences of normal glucose tolerance 94.0%, 80.0%, 54.3% and 58.5% for phenotypes normal, IIA, IIB and IV). CONCLUSION: Affected FCHL family members were more glucose intolerant than non-affected family members. In men, this disturbance was not related to lipid phenotype nor was it explained by obesity.

Adolescent↗

PubMed1979

Impaired feedback control of fat induced gastric inhibitory polypeptide (GIP) secretion by insulin in obesity and glucose intolerance.

To investigate the role of endogenous insulin on the secretion of immunoreactive gastric inhibitory polypeptide (IR-GIP) the response of IR-GIP and immunoreactive insulin (IRI) to an oral fat load (100 g triglyceride) alone and during an intravenous glucose infusion (0.7 g/kg/h) was examined in normal weight and obese subjects. In normal weight subjects the fat induced integrated rise of IR-GIP was 112.7 +/- 9.4 ng/ml/120 min. When glucose and fat were given together this IR-GIP response was lowered to 46.2 +/- 2.9 ng/ml/120 min while the serum IRI response to i.v. glucose and the glucose tolerance were enhanced by fat ingestion. In obese subjects with normal glucose tolerance the GIP suppressing effect of i.v. glucose infusion was less marked than in controls. The integrated IR-GIP response to fat ingestion was 225.6 +/- 20.3 mg/ml/120 min and to fat plus glucose 152.6 +/- 14.8 ng/ml/120 min. In obese subjects with glucose intolerance i.v. glucose completely failed to lower the exaggerated secretion of IR-GIP following oral fat. Thus, a graded abnormality of the GIP response to glucose induced insulin release occurs in obesity with normal and pathological glucose tolerance. After reducing the ideal body weight of six obese subjects with glucose intolerance by hypocaloric diet for 3 weeks the exaggerated rise of IR-GIP after oral fat was reversed and the lowering effect of i.v. glucose on the IR-GIP response re-established.

Adult↗

PubMed1990

Association of plasma triglyceride and C-peptide with coronary heart disease in Japanese-American men with a high prevalence of glucose intolerance.

In a community-based study of second-generation Japanese-American men known to have a high prevalence of both Type 2 (non-insulin-dependent) diabetes and impaired glucose tolerance, there was a highly significant association of coronary heart disease with glucose intolerance in a study sample of 219 men. Intra-abdominal cross sectional fat area determined by computed tomography was significantly elevated in men with coronary heart disease even after adjustment for glucose intolerance and body mass index (p = 0.026). Other differences that were significantly related to coronary heart disease after adjustment for glucose intolerance were lower high density lipoprotein cholesterol levels (p = 0.001), elevated total triglyceride and very low density lipoprotein triglyceride (p less than 0.001), and elevated fasting insulin and C-peptide levels p = 0.001. When these variables were tested in a stepwise multiple logistic regression model, significant independent associations with coronary heart disease were found only for total triglyceride and fasting C-peptide after adjustment for glucose tolerance status. Variables identified to be associated with coronary heart disease were interpreted as representing or manifesting an insulin resistant state. Thus, insulin resistance may be the underlying risk factor aetiologically linking glucose intolerance with coronary heart disease.

Alcohol Drinking↗

PubMed1997

The Santa Barbara County Health Care Services program: birth weight change concomitant with screening for and treatment of glucose-intolerance of pregnancy: a potential cost-effective intervention?

Macrosomic infants still suffer birth trauma in excess of the general population; thus, while debated, the medical and legal sequelae of macrosomia appear to be costly. The clinical role of maternal hyperglycemia below the threshold for the diagnosis of gestational diabetes (GDM) in the etiology of macrosomia remains an area of controversy. Based on the hypothesis that increasing glucose levels result in an increasing prevalence of macrosomia, we designed a study to observe the impact on birth weight and on cost of a treatment program for glucose-intolerant pregnant women in The Santa Barbara County Health Care Services (SBCHCS). In 1985, 18% of 4364 births (85% Mexican-American in origin) in the SBCHCS were > 90th percentile birth weight. In 1986, we began a program to treat all glucose-intolerant pregnant women who had a positive glucose challenge test (GCT > 140 mg/dL after a 50-g oral glucose load), even if they had a negative glucose tolerance test. All glucose-tolerant pregnant women were placed on a 40% carbohydrate, 1800 kcal diet and taught to monitor their blood glucose. Insulin was begun if the fasting blood glucose was > 90 mg/dL and/or the 1-hour post meal was > 120 mg/dL. After introduction of the screening/ treatment program, the prevalence of macrosomia in 1992 was 7% and the cesarean section rate had dropped from 30 to 20%. The cost to SBCHC to educate and treat the additional glucose-intolerant women was $233,650. Assuming that there would have been an additional 398 macrosomic infants with some requiring cesarean delivery and intensive care, total potential savings could be estimated at $833,870 per year. Thus, treatment of glucose-intolerant pregnant women was associated with a decrease in macrosomia and may be cost-effective.

Birth Weight↗

PubMed1988

First-phase insulin response to glucose in nonobese or obese subjects with glucose intolerance: analysis by C-peptide secretion rate.

This study was proposed to clarify the impairment of first-phase insulin response to glucose in subjects with glucose intolerance by analysis of C-peptide secretion rate after glucose or glucagon injection. The rate was calculated from kinetic analysis of peripheral C-peptide behavior. The rate reached the peak two minutes after glucose injection and then rapidly declined (first-phase secretion) in control subjects. In nonobese subjects with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM), the rate promptly increased in response to glucose and was followed by a second phase increase. The time course of the rate in the subjects was slightly different from that in control subjects. There was a progressively greater deficit in the first-phase increase with increasing severity of glucose intolerance. The time course of the rate in the obese subjects with NIDDM was different from that in control subjects. The first-phase increase was reduced in the obese subjects with NIDDM. The glucose disappearance rate was correlated with the first-phase increase. Since the time course of the rate after glucagon injection in all subjects did correspond well with that in the control subjects, variation of metabolic clearance rate of endogenous C-peptide among the subjects may be negligible for this study. This study provides the precise time course of first- and second-phase insulin response to glucose injection in nonobese and obese subjects with IGT or NIDDM as well as convincing evidence of the progressive reduction of first-phase insulin response with increasing severity of glucose intolerance. First-phase insulin response to glucose might be slightly delayed in some obese subjects with NIDDM.

Adult↗

PubMed2000

Recombinant human betacellulin promotes the neogenesis of beta-cells and ameliorates glucose intolerance in mice with diabetes induced by selective alloxan perfusion.

Betacellulin (BTC), a member of the epidermal growth factor family, is expressed predominantly in the human pancreas and induces the differentiation of a pancreatic acinar cell line (AR42J) into insulin-secreting cells, suggesting that BTC has a physiologically important role in the endocrine pancreas. In this study, we examined the in vivo effect of recombinant human BTC (rhBTC) on glucose intolerance and pancreatic morphology using a new mouse model with glucose intolerance induced by selective alloxan perfusion. RhBTC (1 microg/g body wt) or saline was injected subcutaneously every day from the day after alloxan treatment. The intraperitoneal glucose tolerance test revealed no difference between rhBTC-treated and rhBTC-untreated glucose-intolerant mice at 2-4 weeks. However, glucose tolerance was significantly improved and body weight was significantly increased in rhBTC-treated mice compared with untreated mice at 8 weeks. Islet-like cell clusters, consisting mainly of beta-cells, were increased in the pancreas and were localized in contact with the ductal lining cells and sometimes with acinar cells. In conclusion, administration of rhBTC improved glucose tolerance in this mouse model by increasing beta-cell volume, primarily through accelerated neogenesis from ductal lining cells.

Animals↗

PubMed1989

Glucose tolerance in Papua New Guinea: ethnic differences, association with environmental and behavioural factors and the possible emergence of glucose intolerance in a highland community.

That Melanesians of non-Austronesian genetic ancestry may be relatively resistant to glucose intolerance was supported by the results of a study of two semitraditional non-Austronesian villages in the Papua New Guinean highlands in 1983, in which an absence of diabetes and a high degree of glucose tolerance and insulin sensitivity were observed. The second of this series of surveys was conducted in 1985 in three non-traditional communities: a periurban, non-Austronesian village in the highlands, and rural and periurban Austronesian villages in coastal locations. Although an absence of diabetes was demonstrated once again in the highlanders, these periurban subjects showed an unexpectedly high insulin response which may be a precursor of glucose intolerance. The notion that highland communities that are living in non-traditional circumstances in Papua New Guinea presently are in "metabolic transition" towards diabetes and other non-communicable diseases, if correct, is of importance to the public health of the nation. In the periurban, coastal-dwelling Austronesians, diabetes with severe hyperglycaemia was demonstrated, and there was some evidence of a secular trend towards increasing glucose intolerance. The two-hour plasma glucose concentrations were shown to be associated with obesity, modernity and Seventh-Day Adventist religious persuasion. However, important and unexplained differences in glucose tolerance remained between rural and periurban coastal dwellers after taking these factors into account.

Adult↗

PubMed1997

Glucose intolerance after renal transplantation depends upon prednisolone dose and recipient age.

BACKGROUND: Retrospective studies on the prevalence of posttransplant diabetes mellitus (PTDM) in patients on triple-drug immunosuppressive therapy have shown great dispersity, while the incidence of posttransplant impaired glucose tolerance (IGT) is unknown. The aim of our study was to prospectively examine the incidence of posttransplant glucose intolerance and to assess potential risk factors. METHODS: Glucose intolerance was prospectively examined in 173 consecutive kidney transplant recipients by oral glucose tolerance tests (n=167) or the diagnosis of manifest diabetes mellitus (n=6) at 10 weeks after transplant. RESULTS: We found a high incidence of PTDM (18%) and IGT (31%). Univariate analysis revealed that age, family history of diabetes, HLA-B27 phenotype, DR mismatch, rejection, actual prednisolone dose, total methylprednisolone dose, total steroid dose, cytomegalovirus (CMV) infection, and the use of furosemide were associated with PTDM. Age, prednisolone dose, CMV infection, and the use of beta-blockers were associated with IGT. Gender, body mass index, donor source, and cyclosporine level did not influence glucose tolerance. Prednisolone dose, age, family history of diabetes, CMV infection, and HLA-B27 phenotype were independent predictors of PTDM with the use of multiple stepwise logistic regression analysis. Age, prednisolone dose, and the use of a beta-blocker were associated with IGT in the multivariate model. Both univariate and multivariate linear regression analysis revealed a significant relationship between the 2-hr serum glucose and prednisolone dose. The risk of developing PTDM was 5% per 0.01 mg/kg/day of increase in prednisolone dose. CONCLUSIONS: Increased prednisolone dose and older age are strongly associated with the development of posttransplant glucose intolerance.

Adult↗

PubMed1992

Analysis of early-phase insulin responses in nonobese subjects with mild glucose intolerance.

OBJECTIVE: To study the possible contribution of a B-cell defect in the development of glucose intolerance in nonobese subjects. RESEARCH DESIGN AND METHODS: There were 41 normal, nondiabetic subjects; 18 subjects with IGT; and 21 patients with NIDDM. All subjects were nonobese (BMI < 27 kg/m2). Insulin secretory responses to an OGTT, IVGTT, and GST were studied. RESULTS: Early-phase insulin responses to OGTT and IVGTT were decreased in subjects with IGT to levels comparable with those in NIDDM patients, whereas the response to GST was preserved in the subjects with IGT compared with NIDDM patients. The insulinogenic index of OGTT correlated well (r = 0.78) with early-phase insulin response to IVGTT, suggesting that the insulinogenic index in OGTT is related to the early-phase insulin response to IVGTT in nonobese subjects. CONCLUSIONS: Impaired early-phase insulin response to glucose was associated with mild glucose intolerance, suggesting the importance of impaired insulin secretion in the development of glucose intolerance in nonobese subjects.

Blood Glucose↗

PubMed2006

Effect of inhibition of alpha-glucosidase on age-related glucose intolerance and pancreatic atrophy in rats.

Oral administration of alpha-glucosidase inhibitor reduces postprandial serum glucose and insulin concentrations; thus, alpha-glucosidase inhibitor is used for the treatment of diabetes mellitus worldwide. In our study, we have evaluated the effect of alpha-glucosidase inhibitor, acarbose, on age-related glucose intolerance and pancreatic atrophy in the Long-Evans Tokushima Otsuka (LETO) rat. The first group of rats received a standard rat diet (control). The second group received a diet containing acarbose (150 mg/100 g food) from 12 to 28 weeks and then switched to a standard rat diet until 72 weeks of age (A12-28W). The third group was administered the same diet containing acarbose from 12 to 72 weeks of age (A12-72W). Fasting serum glucose and insulin concentrations gradually increased with increasing age in the control group, but these increases were completely prevented (A12-72W) or delayed (A12-28W) by acarbose treatment. In addition, acarbose treatment prevented the deterioration in insulin resistance with increasing age. At 72 weeks of age, pancreatic wet weight and DNA content in the A12-72W group were significantly higher than those in the control group. Although most islets were enlarged, and some portions of pancreatic tissue contained fatty and connective tissue in the control group, these alterations were mild in the A12-28W group and remained minimal in the A12-72W group. Our study suggests that acarbose is useful in the prevention of age-related glucose intolerance and pancreatic atrophy.

Acarbose↗

PubMedDate not supplied

Experimentally induced glucose intolerance increases oral ethanol intake in rats.

A number of studies have shown a relationship between glucose tolerance and ethanol intake. The present study uses a relatively simple procedure to induce glucose intolerance to test whether this condition is sufficient to produce an increase in chronic ethanol intake in male rats. Subjects were divided equally into four groups where they were given access to one of four solutions: peppermint-flavored sucrose (40%), peppermint-flavored saccharin (0.1%), peppermint in water (0.1%), or water alone presented three times a week, for a period of 11 weeks. After 12 weeks all animals were subjected to an oral glucose tolerance test which revealed that the chronically prepared sucrose animals had become glucose intolerant. At the start of week 13 all animals were given access to a 6% ethanol solution flavored with peppermint in place of the previous solutions for a period of 11 weeks. Sucrose animals displayed an immediate preference for ethanol and consumed approximately three times more ethanol than the remaining groups. The results of this study indicate that rats that are made glucose intolerant by long term access to a high concentration of sucrose, when given the opportunity, will subsequently choose to drink more ethanol than control animals.

Alcohol Drinking↗

PubMed1997

Metformin enhances clearance of chylomicrons and chylomicron remnants in nondiabetic mildly overweight glucose-intolerant subjects.

OBJECTIVE: To assess the effect of metformin on the metabolism of intestinally derived lipoproteins in nondiabetic individuals who were mildly overweight and glucose intolerant. RESEARCH DESIGN AND METHODS: A total of nine subjects with a BMI > or = 25 kg/m(2) and fasting serum glucose < or = 6.1 mmol/l and who were glucose intolerant were studied. The subjects underwent a vitamin A fat-loading test before and after a 3-month treatment with 850 mg metformin twice a day. The metabolic behavior of the postprandial lipoproteins was compared with that found in a group of 19 healthy normolipidemic individuals who participated in a previous study. RESULTS: Mean total plasma, chylomicron fraction, and nonchylomicron fraction retinyl palmitate (RP) pretreatment levels were 3.4-fold, 3.59-fold, and 3-fold higher, respectively, in the study group than in the normolipidemic group and were reduced by 50, 56, and 32%, respectively, after 3 months of metformin treatment. The decrease of chylomicron levels after treatment was positively correlated to the fasting triglyceride values before treatment (r = 0.73, P = 0.039) and to the serum insulin level at 120 min of standard glucose loading before treatment (r = 0.91, P = 0.002). CONCLUSIONS: Metformin was shown to be beneficial in the clearance of postprandial lipoproteins in nondiabetic individuals who were mildly overweight and glucose intolerant.

Cholesterol↗

PubMed1990

The significance of glucose intolerance in pulmonary tuberculosis.

We performed a sequential follow-up of oral glucose tolerance tests on 54 Nigerian patients with active pulmonary tuberculosis in order to determine the significance of glucose intolerance in tuberculosis. Twenty-three patients (42.6%) were found to have abnormal results, including three (5.6%) with a diabetic pattern and 20 (37.0%) with impaired glucose tolerance; 15 (75%) of the latter group had normal results after 3 months treatment while one each of the former group was diabetic, intolerant of glucose and normal respectively. Two patients with normal results initially had impaired glucose tolerance at the second test. Three months after full anti-tuberculosis medication, only one of the eight patients with impaired glucose tolerance at the second oral glucose tolerance test remained intolerant of glucose. Only one patient was frankly diabetic. Our results suggest that glucose intolerance in pulmonary tuberculosis is secondary to infection and is reversible.

Adolescent↗

PubMed1978

Association of HLA antigens with glucose intolerance following renal transplantation.

Records of 109 renal transplant patients were reviewed to test the hypothesis that post transplant glucose intolerance would be associated with "diabetic", HLA antigens (HLA--B8, B18, Bw15 and Bw16). Of 42 patients with significant glucose intolerance, 23 had one or more of these antigens (RR=2.65, P=0.01). These findings suggest that stress or drug treatment associated with renal transplantation can induce glucose intolerance in patients with a "diabetic" gene associated with the HLA--B locus.

Cadaver↗

PubMed2003

Obesity, glucose intolerance and diabetes and their links to cardiovascular disease. Implications for laboratory medicine.

This article provides an overview of the role of metabolite toxicity, low-grade inflammation and disturbed cellular signaling in obesity, glucose intolerance and diabetes. It also highlights links between this continuum of deteriorating glucose tolerance and atherosclerosis. Obesity, diabetes mellitus, and cardiovascular disease are all related to diet and to the level of physical activity. They have reached epidemic proportions worldwide. Glucose intolerance and diabetes increase the risk of atherosclerotic events. Moreover, obesity, and glucose intolerance or diabetes, are components of the metabolic syndrome, which also imparts an increased cardiovascular risk. There is increasing recognition that common mechanisms contribute to diabetes and cardiovascular disease. Following increased calorie intake and/or decreased physical activity, fuel metabolism generates excess of 'toxic' metabolites, particularly glucose and fatty acids. Homeostasis is affected by the endocrine output from the adipose tissue. Reactive oxygen species are generated, creating oxidative stress, which exerts major effects on signaling pathways, further affecting cellular metabolism and triggering low-grade inflammatory reaction. This perspective on the diabetic syndrome has been reflected in the approach to its treatment, which integrates maintenance of glycemic control with primary and secondary cardiovascular prevention. Laboratory medicine should support diabetes care with an integrated package of tests which, in addition to glycemic control, enable assessment and monitoring of the risk of microvascular complications as well as cardiovascular disease.

Cardiovascular Diseases↗

PubMed2006

Isoprostanes, a marker of lipid peroxidation, may not be involved in the development of glucose intolerance.

We investigated whether isoprostanes, as a marker of lipid peroxidation, may be involved in the development of impaired glucose tolerance (IGT) or diabetes. Using a nested case-control study, we tracked the changes in isoprostane levels, insulin sensitivity (IS) and beta-cell function (BCF) in Afro-Jamaicans who progressed to IGT and diabetes over 3.9 years. Anthropometry, glucose tolerance, insulin levels, blood pressure and urinary isoprostane concentration were measured at baseline and follow-up. IS and BCF were estimated by the method of homeostasis assessment. Fifty-two individuals who progressed to IGT or diabetes and 44 age, sex and body mass index (BMI) matched controls were studied. Progression to glucose intolerance was significantly related with baseline BCF (p< or =0.01), but not isoprostane levels or IS. Glucose concentrations (fasting and 2 h) on follow-up were significantly correlated to baseline IS, baseline BCF, follow-up IS and follow-up BCF (p-values<0.05). In multiple regression analysis, only follow-up IS and BCF (p-values< or =0.001) independently predicted fasting glucose and 2h glucose levels at follow-up. Isoprostanes were not significantly associated with IS or BCF (p-values>0.1). We concluded that isoprostanes may not be causally involved in the development of glucose intolerance, insulin resistance or deteriorating BCF.

Adult↗

PubMed2005

Cameroon local diet-induced glucose intolerance and dyslipidemia in adult Wistar rat.

It has been hypothesised that glucose intolerance or diabetes can be induced in rodents by a hypercaloric-fat diet or a hypercaloric-sucrose diet. This study was designed to examine the effects of a high-fat diet (HFD: carbohydrates 35-40% kcal, fat 50-55% kcal, protein 10-15% kcal) and a high-sucrose diet (HSD: carbohydrates 65-70% kcal, fat 25-30% kcal, protein 10-15% kcal) compared to a normal or standard diet (ND: carbohydrates 50-55% kcal, fat 15-20% kcal, protein 25-30% kcal) on fasting plasma glucose, glucose tolerance test, plasma triglycerides, plasma cholesterol, body weight, food and water consumption in male Wistar rats. After 4 months, weight gain, plasma triglycerides level, fasting plasma glucose and water intake were significantly elevated (p<0.05) in all test groups when compared to the control group. Total HDL and LDL cholesterol levels were significantly elevated (p<0.05) in the HFD group, whereas the HDL level was significantly lower in the HSD group associated with an atherogenic index significantly elevated (p<0.05) when compared to the control group. After 16 weeks of dietary treatment, an oral glucose tolerance test (OGTT) showed a significant increase in plasma glucose levels after 2-4 h of glucose challenge in all test groups. During the experiment, it was noticed that important weight gain observed in all dietary test groups was associated with a significant low (p<0.05) food consumption. The above results suggest that dietary nutrients contained in these hypercaloric diets might have an effect on insulin action and therefore, might contribute to the development of glucose intolerance and type 2 diabetes. These results also suggest that, in addition to their diabetogenic effect, these hypercaloric diets might probably have an atherogenic effect and could be use in a long-term study to induce type 2 (non-insulino-dependant) diabetes mellitus.

Animals↗

PubMed1985

Role of parathyroid hormone in the glucose intolerance of chronic renal failure.

Evidence has accumulated suggesting that the state of secondary hyperparathyroidism and the elevated blood levels of parathyroid hormone (PTH) in uremia participate in the genesis of many uremic manifestations. The present study examined the role of PTH in glucose intolerance of chronic renal failure (CRF). Intravenous glucose tolerance tests (IVGTT) and euglycemic and hyperglycemic clamp studies were performed in dogs with CRF with (NPX) and without parathyroid glands (NPX-PTX). There were no significant differences among the plasma concentrations of electrolytes, degree of CRF, and its duration. The serum levels of PTH were elevated in NPX and undetectable in NPX-PTX. The NPX dogs displayed glucose intolerance after CRF and blood glucose concentrations during IVGTT were significantly (P less than 0.01) higher than corresponding values before CRF. In contrast, blood glucose levels after IVGTT in NPX-PTX before and after CRF were not different. K-g rate fell after CRF from 2.86 +/- 0.48 to 1.23 +/- 0.18%/min (P less than 0.01) in NPX but remained unchanged in NPX-PTX (from 2.41 +/- 0.43 to 2.86 +/- 0.86%/min) dogs. Blood insulin levels after IVGTT in NPX-PTX were more than twice higher than in NPX animals (P less than 0.01) and for any given level of blood glucose concentration, the insulin levels were higher in NPX-PTX than NPX dogs. Clamp studies showed that the total amount of glucose utilized was significantly lower (P less than 0.025) in NPX (6.64 +/- 1.13 mg/kg X min) than in NPX-PTX (10.74 +/- 1.1 mg/kg X min) dogs. The early, late, and total insulin responses were significantly (P less than 0.025) greater in the NPX-PTX than NPX animals. The values for the total response were 143 +/- 28 vs. 71 +/- 10 microU/ml, P less than 0.01. There was no significant difference in the ratio of glucose metabolized to the total insulin response, a measure of tissue sensitivity to insulin, between the two groups. The glucose metabolized to total insulin response ratio in NPX (5.12 +/- 0.76 mg/kg X min per microU/ml) and NPX-PTX (5.18 +/- 0.57 mg/kg X min per microU/ml) dogs was not different but significantly (P less than 0.01) lower than in normal animals (9.98 +/- 1.26 mg/kg X min per microU/ml). The metabolic clearance rate of insulin was significantly (P less than 0.02) reduced in both NPX (12.1 +/- 0.7 ml/kg X min) and NPX-PTX (12.1 +/- 0.9 ml/kg X min) dogs, as compared with normal animals (17.4 +/- 1.8 ml/kg X min). The basal hepatic glucose production was similar in both groups of animals and nor different from normal dogs; both the time course and the magnitude of suppression of hepatic glucose production by insulin were similar in both in groups. There were no differences in the binding affinity, binding sites concentration, and binding capacity of monocytes to insulin among NPX, NPX-PTX, and normal dogs. The data show that (a) glucose intolerance does not develop with CRF in the absence of PTH, (b) PTH does not affect metabolic clearance of insulin or tissue resistance to insulin in CRF, and (c) the normalization of metabolism in CRF in the absence of PTH is due to increased insulin secretion. The results indicate that excess PTH in CRF interferes with the ability of the beta-cells to augment insulin secretion appropriately in response to the insulin-resistant state.

Animals↗