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Results for “Glucose Intolerance”

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PubMed1996

Decreased insulin-mediated but not non-insulin-dependent glucose disposal rates in glucose intolerance and type II diabetes in African (Ghanaian) immigrants.

The authors evaluated the significance of beta cell function, non-insulin-dependent glucose disposal (glucose effectiveness [Sg]), and insulin-dependent glucose disposal (insulin sensitivity) in African immigrants with varying degrees of glucose tolerance. Thirty-two African immigrants residing in Franklin County, Ohio, were studied. There were 16 subjects with normal glucose tolerance (NGT), 11 with intermediate glucose tolerance (IGT), and 5 with type II diabetes mellitus (DM). Insulin sensitivity index and Sg were measured by an insulin-modified, frequently sampled intravenous glucose tolerance test. The mean fasting and post-glucose serum glucose levels were lowest in the NGT, intermediate in the IGT group, and highest in the DM group. Mean serum insulin and c-peptide responses rose briskly by threefold to a peak in the NGT and the IGT groups. In the DM group, mean serum insulin and c-peptide responses were severely blunted to glucose stimulation. The sensitivity index was highest in the NGT (3.09 +/- 0.27), intermediate in the IGT (1.81 +/- 0.47), and lowest in the DM (0.48 +/- 0.28 x 10(-2).mins-1 (microU/ml)-1). The Sg was identical in the NGT (2.78 +/- 0.22) and IGT (2.78 +/- 0.27) groups but was slightly but not significantly lower in the DM (2.20 +/- 0.35 x 10(-2).mins-1). In addition, the glucose decay constant was not statistically different in the NGT (3.00 +/- 0.38) and IGT (2.25 +/- 0.19) group, but the mean values were significantly greater than in the patients with diabetes (0.78 +/- 0.15 percent/mins). The mean disposition index (sensitivity index X beta cell function as assessed by both insulin and c-peptide) was significantly greater in NGT than in the IGT (P<0.05) and in the diabetic group (P<0.001). In summary, the authors demonstrate that, in native African immigrants, type II diabetes is associated with significant reduction in beta cell function, insulin sensitivity, and glucose decay constant, but not in Sg. In patients with intermediate or impaired glucose tolerance, there is moderate insulin resistance and evidence of inadequate compensation by beta cell, but the Sg, the Sg at theoretical insulin concentration, and glucose decay constant remain normal. They conclude that, unlike other ethnic and racial groups, in glucose intolerant native African patients, alterations in Sg or non-insulin dependent glucose disposal (ie, tissue glucose sensitivity) do not appear to play a significant role in the impairment of glucose tolerance and type II diabetes in African immigrants.

Adult↗

PubMed1981

Plasma insulin and C-peptide in normal and glucose intolerant males: the role of hepatic insulin uptake.

Plasma immunoreactive insulin and peptide were measured in the basal and glucose-stimulated state in middle-age males. Normals were compared with individuals with mild to moderate glucose intolerance. Ths results demonstrate the value of C-peptide measurements in the assessment of "true" insulin secretion and suggest that a reduced hepatic insulin extraction is a feature of the glucose intolerant state.

C-Peptide↗

PubMed1987

MTP-1307, a novel antidiabetic agent, improves the glucose intolerance of viable yellow obese-diabetic mice.

MTP-1307 is an oral antidiabetic agent with a unique profile. It improves the glucose intolerance of viable yellow obese-diabetic mice at 25 mg/kg whereas at 300 mg/kg, it only marginally lowers the basal glucose levels of the same mice. This selective activity on exogenous glucose makes MTP-1307 potentially a useful agent to treat postprandial glucose intolerance without causing hypoglycemia.

Animals↗

PubMed1995

The relationship between insulin resistance and insulin secretion in Japanese subjects with borderline glucose intolerance.

Insulin resistance and impaired insulin secretion can be involved in the development of non-insulin-dependent diabetes mellitus (NIDDM), but their relative importance or temporal relationship are poorly understood. To elucidate this issue, we studied 51 subjects with borderline glucose intolerance (BGI) and 18 normal glucose tolerant subjects (NGT) according to the Japan Diabetes Society criteria. The glucose infusion rate (GIR, mg/kg/min), an index of whole body insulin resistance (IR), was measured by the euglycemic (80 mg/dl) hyperinsulinemic clamp technique (insulin infusion rate 1.12 mU/kg/min). Insulinogenic index (delta IRI/delta BS at 30 min) and the insulin area under the curve during a 75-g oral glucose tolerance test (OGTT) were estimated. In the BGI subjects, the GIR values showed marked variation ranging from 2.24 to 10.44 mg/kg/min (5.54 +/- 0.31, mean +/- S.E.M.). The GIR values were lower in obese BGI subjects compared with non-obese BGI and NGT subjects, and the insulin area was markedly higher in BGI subjects with increased insulin resistance. There was a significant negative correlation between the GIR values and the insulin area or delta IRI/delta BS (30') ratio in the subjects with BGI either in the whole group or solely in the non-obese group. We conclude that the increased insulin secretion compensates for the peripheral insulin resistance of subjects with slightly deteriorated glucose tolerance, implying that insulin resistance plays an important role in the pathogenesis of NIDDM in some fraction of Japanese population.

Adolescent↗

PubMed2005

The association between maternal obesity, glucose intolerance and hypertensive disorders of pregnancy in nondiabetic pregnant women.

OBJECTIVE: The aim of this study is to evaluate whether pregnancy-induced hypertension (PIH) among nondiabetic patients is associated with glucose intolerance. MATERIALS AND METHODS: A retrospective case-control study was designed including a study group who had pregnancy-induced hypertension or preeclampsia. Patients with normal pregnancy were used as a control group matched to cases by parity. Diabetic patients, nonsingleton pregnancies, and women without prenatal care were excluded. Data concerning fasting glucose levels, glucose challenge test (GCT), and oral glucose tolerance test (OGTT) were collected from patients' files. RESULTS: There were 131 patients in each study group. The study group had significantly higher mean maternal age, mean GCT levels, and mean pregestational body mass index (BMI) (28.0 +/- 5.8 vs. 26.5 +/- 5.3, p = 0.02; 5.8 +/- 1.4 vs. 5.1 +/- 1.1 p = 0.0018; 26 +/- 5.1 vs. 23 +/- 4.0 p < 0.001, respectively) than the control group. Mean gestational age and birthweight were also significantly lower in the study group (38.5 +/- 2.1 vs. 39.4 +/- 1.7 p < 0.001; 2929 g +/- 614.7 vs. 3225 +/- 461.1 p < 0.001, respectively). Stratified analysis according to parity demonstrated that pregestational BMI, weight gain during pregnancy, and cesarean section (CS) were significantly higher in women with pregnancy-induced hypertension than in controls in all parity groups. Maternal age and mean GCT levels of women with pregnancy-induced hypertension were higher in all parity groups but statistically significant only among multiparous patients. Multiple logistic regression demonstrated that BMI, weight gain, and maternal age were independently associated with pregnancy-induced hypertension, while GCT level was not. Conclusions. Elevated pregestational BMI is an independent risk factor for development of pregnancy-induced hypertension (PIH). Its association with elevated GCT levels implies that even without overt diabetes, glucose intolerance may play a role in the pathogenesis of preeclampsia in obese patients.

Adult↗

PubMed1995

Changes in carnitine metabolism with ketone body production in obese glucose-intolerant patients.

To elucidate the relationship between carnitine metabolism and plasma ketone body concentrations in moderately obese patients with mild glucose intolerance, the ketone body and carnitine levels in the basal state were determined in 72 obese patients: 20 with normal glucose tolerance (NGT), 29 with impaired glucose tolerance (IGT), and 23 with non-insulin-dependent diabetes mellitus (NIDDM) having a fasting plasma glucose (FPG) level of less than 200 mg/dl. Total ketone body (TKB) levels significantly (P < 0.05) increased in the order of NGT, IGT, NIDDM, while the FPG and free fatty acid (FFA) concentrations were significantly (P < 0.05) higher in the NIDDM group than in the other two groups. In contrast, the insulin, glucagon and glycerol levels were comparable in the three groups. The plasma short-chain acylcarnitine (SCAC) concentration and the acylcarnitine/free carnitine (AC/FC) ratio were similar in the IGT and NIDDM groups, and significantly (P < 0.05) greater than those in the NGT group. The AC/FC ratio correlated significantly with the FPG and FFA, but not with the TKB. These results suggest that the combination of IGT with simple obesity may trigger the acceleration of hepatic ketogenesis in conjunction with an elevated SCAC and an increased AC/FC ratio. In addition, the data also imply that, in patients with mild NIDDM, factors other than the carnitines may play a greater role in enhancing ketonemia.

Acylation↗

PubMed1993

Association of early-onset coronary heart disease in South Asian men with glucose intolerance and hyperinsulinemia.

BACKGROUND: Rates of coronary heart disease are higher in South Asians (Indians, Pakistanis, and Bangladeshis) settled overseas than in other ethnic groups. We tested the hypothesis that this excess risk results from metabolic disturbances associated with insulin resistance. METHODS AND RESULTS: There were 1,421 South Asian men and 1,515 European men aged 40-69 years in London examined in the Southall Study. Prevalence of ischemic ECG abnormalities was higher in South Asians than in Europeans (17% versus 12%, p < 0.001), with an excess of major Q waves (Minnesota codes 1-1 or 1-2) in younger South Asian men (p = 0.01 for the age-ethnicity interaction). Major Q waves were strongly associated with glucose intolerance and hyperinsulinemia in younger South Asians; these factors accounted statistically for 73% of major Q waves in those aged 40-54 years. Age-standardized prevalence of a positive history of coronary heart disease was similar in South Asians and Europeans (8.5% versus 8.2%, NS), and positive history without Q waves was not associated with glucose intolerance or hyperinsulinemia in South Asians. Smoking rates and average plasma cholesterol were lower in South Asians than in Europeans; in a logistic model controlling for smoking and cholesterol, the odds ratio for major Q waves in South Asians compared with Europeans was 2.4 (95% CI, 1.5-3.8). Adjusting for glucose intolerance and hyperinsulinemia reduced this ratio to 1.5 (95% CI, 0.9-2.5). CONCLUSIONS: These results are consistent with the hypothesis that insulin resistance underlies the high coronary risk in South Asian people and strengthen the evidence for a fundamental role of this metabolic pattern in the etiology of coronary heart disease.

Adult↗

PubMed2002

[Comparison of ADA and WHO diagnostic criteria for diabetes diagnosis and other categories of glucose intolerance ].

UNLABELLED: New diagnostic criteria for diabetes mellitus announced by ADA in 1997 and WHO in 1998 recommend lowering of the fasting plasma glucose to 7.0 mmol/l and introduce new category: impaired fasting glucose. In contrast to ADA, WHO recommends to maintain oral glucose tolerance test in clinical practice. In this study, based on oral glucose tolerance test results and WHO 1998 criteria we estimated diagnostic value of fasting glucose in diagnosing diabetes. The aim of the study was also to compare prevalence of diabetes and other categories of glucose intolerance according to ADA 1997, WHO 1985 and WHO 1998 criteria. METHODS: Oral glucose tolerance test (OGTT) was performed in 1528 patients (785 men, 743 women). According to ADA 1997, WHO 1985 and WHO 1998 criteria the patients were divided into groups depending on glucose tolerance abnormalities. RESULTS: Prevalence of diabetes according to ADA 1997 and WHO 1985 criteria was almost the same, being 10.47% and 10.34%, respectively, and according to WHO 1998 criteria it was 13.15%. In 20.4% of all the patients with diabetes according to WHO 1998 criteria, the diagnosis was made on the basis of 2-h post load glucose, in case of WHO 1985 criteria the percentage was 39.9%. 13.04% of patients with IFG according to ADA had diabetes and 34.06% had IGT according to WHO 1998 criteria. The highest overall percentage agreement (97.19%) was found between WHO 1998 and WHO 1985 classifications with the hypothesis that unclassified group according to WHO 1985 corresponds to IFG group according to WHO 1998. CONCLUSIONS: Despite lower diagnostic value of 2-hour post-load glycaemia in diagnosing diabetes according to WHO 1998 criteria compared to WHO 1985 criteria, OGTT remains irreplaceable diagnostic tool, especially in high risk populations. In patients with IFG according to ADA OGTT causes significant improvement in detecting diabetes.

Blood Glucose↗

PubMed1978

Peripheral neuropathy in myotonic dystrophy. Relation to glucose intolerance.

Motor nerve conduction velocity (MNCV) was measured in three peripheral nerves in each of 24 patients with myotonic dystrophy having various degress of associated glucose intolerance and was compared with results in a control group. Both groups had similar glucose tolerance and were matched for age and adiposity. The mean MNCV in the ulnar, median, and peroneal nerves in the myotonic dystrophy group were all significantly slowed (P less than .01). This peripheral nerve dysfunction, usually subclinical, is yet another manifestation of this multisystem disease and is unrelated to the associated glucose intolerance.

Adult↗

PubMed2003

Prevalence and concomitants of glucose intolerance in European obese children and adolescents.

OBJECTIVE: The worldwide increase in the prevalence of childhood obesity is reaching epidemic proportions and is associated with a dramatic rise in cases of type 2 diabetes. The prevalence of glucose intolerance and its determinants and the relation of cardiovascular risk factors with levels of glycemia and degree of obesity were studied in grossly obese children of European origin. RESEARCH DESIGN AND METHODS: A total of 710 grossly obese Italian children (SD score [SDS] of BMI 3.8 +/- 0.7) aged 6-18 years, including 345 male subjects, underwent an oral glucose tolerance test. Insulin resistance and insulin secretion were estimated using the homeostasis model assessment for insulin resistance and the insulinogenic index, respectively. Fibrinogen, C-reactive protein, lipids, and uric acid were measured. The 2-h postload glucose and degree of obesity, calculated as the SDS of weight/height(2), were used as dependent variables. RESULTS: The prevalence of glucose intolerance was 4.5%. Insulin resistance (P < 0.0001), impaired insulin secretion (P < 0.0001), and diastolic blood pressure (BP) (P < 0.05) were significantly and independently related to 2-h postload glucose values. The degree of obesity did not relate to insulin resistance but was independently correlated with inflammatory proteins, uric acid, and systolic BP, variables that were often abnormal in this population. CONCLUSIONS: In these grossly obese children, both insulin resistance and impaired insulin secretion contribute to the elevation of glycemia, and the degree of obesity is related to cardiovascular risk factors independently of insulin resistance.

Adolescent↗

PubMed1995

Effects of heparin-induced non-esterified free fatty acid on minimal model-derived insulin sensitivity in individuals with varying degrees of glucose intolerance.

The effects of heparin-induced non-esterified free fatty acid (NEFA) release on insulin sensitivity index were studied in individuals with varying degrees of glucose intolerance and beta cell dysfunction during the frequently sampled intravenous glucose tolerance test (IVGTT). The groups comprised: Group 1 (n = 5): newly diagnosed Type 2 diabetic patients, Group 2 (n = 11): impaired glucose tolerance patients (IGT), and Group 3 (n = 16): healthy normal glucose tolerance subjects. The serum insulin and c-peptide levels were severely blunted in the diabetic patients when compared to both non-diabetic groups. Mean fasting and post-heparin plasma NEFA levels were approximately 1.8 fold greater (p < 0.05) in the diabetic patients when compared to the other two groups. The mean insulin sensitivity index was lowest in the diabetic patients, intermediate in the IGT patients, and highest in the healthy controls. A significant negative relationship was found between the insulin sensitivity index and stimulated NEFA (r = -0.537, p < 0.008) but not with the fasting NEFA levels in our subjects. In summary, the frequently sampled IVGTT protocol that employs heparin flushes results in marked elevations in NEFA in Type 2 diabetic patients with poor beta cell dysfunction but not in subjects with intermediate or normal glucose tolerance. The higher plasma NEFA levels during heparin injections could worsen the model-derived, insulin sensitivity index and could impair the ability to achieve an acceptable modelling in Type 2 diabetic patients. We therefore suggest heparin should be avoided in such patients when using this protocol.

Adult↗

PubMed2005

Enhanced glucagon-like peptide-1 (GLP-1) response to oral glucose in glucose-intolerant HIV-infected patients on antiretroviral therapy.

OBJECTIVES: We investigated whether the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which are major regulators of glucose tolerance through the stimulation of insulin secretion, contribute to impaired glucose tolerance (IGT) among HIV-infected patients on highly active antiretroviral therapy (HAART). METHODS: Eighteen HIV-infected male patients (six lipodystrophic and 12 nonlipodystrophic) with normal glucose tolerance (NGT) were compared with 10 HIV-infected male patients (eight lipodystrophic and two nonlipodystrophic) with IGT. Plasma concentrations of GLP-1 and GIP were determined frequently during a 3-h, 75-g glucose tolerance test. Insulin secretion rates (ISRs) were calculated by deconvolution of C-peptide concentrations. RESULTS: The incremental area under the curve (incrAUC) for GLP-1 was increased by 250% in IGT patients compared with NGT patients (1455+/-422 vs. 409+/-254 pmol/L/180 min, respectively; P<0.05), whereas the incrAUC for GIP did not differ between the study groups (7689+/-1097 vs. 8041+/-998 pmol/L/180 min, respectively; not significant). In pooled study groups, the GIP incrAUC correlated positively with the ISR incrAUC without adjustment (r=0.38, P<0.05) and following adjustment for glucose incrAUC (r=0.49, P<0.01). CONCLUSIONS: Our data suggest: (1) that glucose-intolerant, HIV-infected male patients may display enhanced GLP-1 responses to oral glucose compared with normal glucose-tolerant HIV-infected male patients, which may represent a compensatory mechanism rather than explain the IGT; (2) that the GIP response may be associated with ISR independently of plasma glucose in nondiabetic HIV-infected males on HAART.

Adult↗

PubMed2000

Chronic infusion of norepinephrine into the VMH of normal rats induces the obese glucose-intolerant state.

Increases in ventromedial hypothalamic (VMH) norepinephrine (NE) levels and/or activities have been observed in a variety of animal models of the obese insulin-resistant condition. This study examined the metabolic effects of chronic NE infusion (25 nmol/h) into the unilateral VMH of normal rats. Within 4 days, VMH NE infusion significantly increased plasma insulin (140%), glucagon (45%), leptin (300%), triglyceride (100%), abdominal fat pad weight (50%), and white adipocyte lipogenic (100%) and lipolytic (100%) activities relative to vehicle-infused rats. Furthermore, isolated islet insulin secretory response to glucose (15 mM) within 4 days of such treatment was increased over twofold (P < 0.05). Among treated animals, fat stores continued to increase over time and plateaued at approximately 2 wk (3-fold increase), remaining elevated to the end of the study (5 wk). By week 4 of treatment, NE infusion induced glucose intolerance as evidenced by a 32% increase in plasma glucose total area under the glucose tolerance test curve (P < 0.01). Whole body fat oxidation rate measured after 5 wk of infusion was significantly increased among treated animals as evidenced by a reduced respiratory quotient (0.87 +/- 0.01) relative to controls (0. 90 +/- 0.01). VMH NE infusion induced hyperphagia (30%) only during the first week and did not affect body weight over the 5-wk period. Increases in VMH NE activity that are common among obese insulin-resistant animal models can cause the development of this obese glucose-intolerant (metabolic) syndrome.

Adipose Tissue↗

PubMed1994

Glucokinase gene polymorphisms: a genetic marker for glucose intolerance in a cohort of elderly Finnish men.

Although mutations in the glucokinase gene are implicated in the pathogenesis of glucose intolerance in pedigrees with maturity-onset diabetes of the young, the role of such mutations in typical Type 2 diabetes is poorly characterized. We studied a cohort of elderly men born (between 1900 and 1919) in two Finnish communities and exhibiting a continuous spectrum of glucose tolerance at assessments made in 1984 and 1989. Individuals were typed at two polymorphic microsatellites straddling the glucokinase gene, GCK(3') (n = 169) and GCK(5') (n = 166): these two markers were in linkage equilibrium in this cohort. Significant associations between alleles at the GCK(3') marker and glucose tolerance were evident (p = 0.002), the frequency of the (z + 2) allele rising from zero in control subjects (n = 88 chromosomes) to 6.5% (n = 62) in subjects with impaired tolerance and 12.2% (n = 188) in subjects with diabetes. Mean 2-h glucose levels were 10.5 (9.6-11.4, 95% confidence interval) mmol l-1 in individuals with the (z + 2) allele and 8.1 (7.6-8.7) mmol l-1 in those without (p = 0.01, corrected for multiple comparisons). No association was evident between GCK(5') alleles and glucose tolerance. The GCK(3') microsatellite is a marker for abnormal glucose tolerance in this cohort of elderly Finnish men.

Aged↗

PubMed1995

Prevalence of macro- and microvascular diseases in non-insulin-dependent diabetic and borderline glucose-intolerant subjects with insulin resistance syndrome.

This study was undertaken to ascertain whether patients with insulin resistance syndrome, a cluster of risk factors for coronary artery disease (CAD), are really a high risk population for macro- and microvascular diseases in Japanese NIDDM and borderline glucose-intolerant subjects. A diagnosis of insulin resistance syndrome was made if four of the six following criteria are satisfied: glucose disposal rate < 2.2 mg/kg/min, fasting plasma IRI > 15 microU/ml or peak plasma IRI > 100 microU/ml during meal tolerance test, plasma triglyceride > 150 mg/dl at fasting or > 200 mg/dl after meal, serum HDL-cholesterol < 40 mg/dl, blood pressure > 140 mm Hg systolic and > 90 mm Hg diastolic or treatment with antihypertensive agents, and body mass index (BMI) > 27 for men or > 25 for women. We compared the prevalence of CAD, cerebral vascular disease (CVD), peripheral vascular disease (PVD), retinopathy and nephropathy between the insulin resistance syndrome group (group A, n = 57) and the remaining group (group B, n = 164). Both groups did not differ with respect to age, duration of diabetes, BMI, fasting plasma glucose, HbA1c, composition of NIDDM and borderline glucose-intolerance (BGI) or treatment modality. The prevalence of CAD was significantly higher in group A compared with that in group B (31.6% vs. 14.0%, P < 0.002), but not for CVD (8.8% vs. 3.7%, respectively, P = 0.12) or PVD (1.8% vs. 2.4%, respectively, P = 0.76). The prevalence of late-stage retinopathy in group A was significantly higher than that in group B (12.3% vs. 2.4%, respectively, P < 0.005). Macroalbuminuria, but not microalbuminuria, was significantly higher in group A than that in group B (12.3% vs. 3.6%, P < 0.02). We conclude that the insulin resistance syndrome preferentially increases the development of CAD, and is also involved in the progression of microvascular diseases.

Adult↗

PubMed1987

Relationships between insulin secretion, insulin metabolism and insulin resistance in mild glucose intolerance.

The aim of this study was to evaluate whether the correlation between insulin resistance and peripheral hyperinsulinaemia existing in mild glucose intolerance corresponds to a relationship between insulin resistance and insulin overproduction by the pancreas. In addition, the possibility that insulin resistance is related to insulin metabolism was examined. Twenty five subjects with fasting normoglycaemia and an abnormal glucose response to the oral glucose tolerance test (OGTT) were studied. Insulin secretion by the pancreas was estimated by means of fasting C-peptide levels in peripheral blood. Insulin resistance was estimated by the rate of glucose disappearance from plasma after i.v. insulin injection. Insulin metabolism was estimated indirectly by the C-peptide: insulin molar ratio. A negative correlation was found between the glucose disappearance rate from plasma after i.v. insulin injection and fasting insulin levels (r = -0.677, p less than 0.001), but not fasting C-peptide concentrations (r = -0.164, p = NS). Glucose disappearance rate from plasma correlated positively with the C-peptide: insulin molar ratio (r = 0.626, p less than 0.001). These results suggest that in mild glucose intolerance insulin resistance and insulin secretion by the pancreas are not related phenomena, and that the defect responsible for insulin resistance might also be implicated in the impaired insulin metabolism.

Adult↗

PubMedDate not supplied

[Limitations of the diagnostic criteria for type 2 diabetes and glucose intolerance].

Conflicting results have been published during the past three decades regarding the cut points for the diagnosis of diabetes and glucose intolerance. Two major consensus changed the diagnostic values; the last revision occurred in 1997. After the publication of the new criteria, the controversy grew. New evidence was published demonstrating that the new cut points were inappropriate. The purpose of this review paper is to summarize the currently available information useful to evaluate the sensibility and specificity of the diagnostic criteria and to discuss the difficulties to define properly the cut-points for the diagnosis of diabetes and glucose intolerance.

Aged↗

PubMed1986

Risks for glucose intolerance.

Cardiovascular disease is the major cause of morbidity and mortality in diabetics. In this article, the prevalence of cardiovascular disease in diabetes is described, and the factors that influence the development of cardiovascular disease are explored. The interaction of other risk factors for cardiovascular disease and glucose intolerance and the question of whether glucose intolerance is truly an independent risk factor are also discussed.

Blood Glucose↗