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PubMed2006

Comparative neurophysiological study for the diagnosis of mild polyneuropathy in patients with diabetes mellitus and glucose intolerance.

This article evaluates diagnostic sensitivity of minimal F-wave latency, sural/radial amplitude ratio (SRAR), dorsal sural/radial amplitude ratio (DSRAR), sympathetic skin response (SSR), and R-R interval variability (RRIV) for detecting early polyneuropathy in patients with glucose intolerance and diabetic patients. F-wave latencies were more prolonged in diabetic patients with normal and abnormal nerve conduction studies than control subjects (p < .001). SRAR was lower, SSR latency was more prolonged, and RRIV was lower in diabetic patients with abnormal nerve conduction studies than healty controls (p < .001). SSR latency was more prolonged and RRIV was lower in diabetic patients with normal nerve conduction studies than healty controls (p < .01, p < .05, respectively). DSRAR was lower in diabetic patients with normal and abnormal nerve conduction studies than control subjects (p < .001). DSRAR was also lower in patients with glucose intolerance than control subjects (p < .01). DSRAR was the most sensitive and specific test in either of diabetic patients with normal nerve conduction studies (sensitivity 66%, specificity 90%) and diabetic patients with abnormal nerve conduction studies (sensitivity 100%, specificity 90%). DSRAR is the most reliable method for detection of early nerve pathology. Patients with glucose intolerance might have subclinical neuropathy that can be demonstrated with DSRAR analysis.

Adult↗
PubMed1984

Oral contraceptive use: prospective follow-up of women with suspected glucose intolerance.

593 women from a cohort of 8,652 healthy women failed a 1-hr glucose screening test. These 593 women with suspected glucose intolerance were classified as normal or as having impaired glucose tolerance (IGT) or diabetes mellitus (DM) after an oral standard glucose tolerance test (SGTT) and were followed over a mean 8.55 years. No permanent change in glucose status as a result of oral contraceptive use was found in an analysis for impaired glucose tolerance, diabetes mellitus, diabetic symptoms, or use of oral agents and/or insulin. Increased glucose intolerance was observed for women who were older, had a positive family history of diabetes, or were of greater relative weight. Diabetic symptoms correlated most closely with the onset of persistent fasting hyperglycemia.

Adolescent↗
PubMed1986

Physiologic and cellular insulin action in a glucose-intolerant model of type 2 (non-insulin-dependent) diabetes in rats.

A B-cell-deficient model for Type 2 (non-insulin-dependent) diabetes mellitus has been investigated with regard to insulin action at the cellular level. Two-day-old male Sprague Dawley rats were injected with streptozotocin (90 mg/kg) or citrate buffer. At 6 weeks streptozotocin-treated animals were hyperglycaemic and exhibited glucose intolerance, e.g. at 45 min post-glucose (1.5 g/kg) the change in serum glucose level from baseline was 6 +/- 7 mg% in control rats vs. 212 +/- 18 mg% for the streptozotocin-treated rats. Basal activity and insulin action in isolated adipocytes, as estimated by 2-deoxyglucose uptake and glucose metabolism, were not influenced by streptozotocin treatment. For example, uptake of 0.1 mmol/1 2-deoxyglucose at 1000 microU insulin/ml was 58 +/- 8 pmol/10(5) cells min-1 vs 54 +/- 6 pmol for adipocytes isolated from experimental vs. control animals. Although serum insulin levels in streptozotocin-treated rats were significantly decreased (p less than 0.05), there was no difference in insulin receptor number or affinity. Glucose intolerance present in this model is similar to that in Type 2 diabetes. However, concomitant insulin intolerance was not observed. Taken together with our findings of unaltered insulin action at the cellular level, this suggests that the pathogenesis of insulin resistance is not dependent on glucose intolerance. Moreover, this hyperglycaemic model is responsive to oral hypoglycaemic agents and can be used to establish their direct effects on physiologic and cellular insulin action.

Adipose Tissue↗
PubMed1991

Glucose intolerance and diabetic complications among Japanese-American women.

The prevalence of glucose intolerance and diabetic complications was determined in second-generation Japanese-American (Nisei) women and compared to previously obtained results in Nisei men. A volunteer study sample of 191 Nisei women 45-74 years old was enrolled from a study population of 1489 Nisei women born 1913-1942, raised and educated in the U.S., and residing in King County, Washington. The enrolled sample included 72 with normal glucose tolerance, 67 with impaired glucose tolerance (IGT), and 52 with non-insulin-dependent diabetes. A random sample was also drawn from the study population to form a reference sample of 157 women. Based upon observations in the reference and enrolled samples, an estimated 16% of Nisei women in the study population have diabetes and 40% IGT. These rates compare to 20% diabetes and 36% IGT previously estimated for Nisei men 45-74 years old. The prevalence of cardiovascular disease (hypertension, peripheral vascular disease, and/or coronary heart disease) was highest among diabetic women, lowest in those with normal glucose tolerance, and intermediate in women with IGT. In comparison to diabetic men, there was a significantly lower frequency of neuropathy, peripheral vascular disease, and coronary heart disease in diabetic women. However, hypertension occurred equally often in both. Thus Japanese-American men and women 45-74 yr old have a similar prevalence of glucose intolerance, although less severe in women, and complications, except for hypertension, are reduced in women.

Adult↗
PubMed2003

Glucose intolerance, insulin resistance, and hyperandrogenemia in first degree relatives of women with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is associated with hyperinsulinemia, insulin resistance (IR), increased risk of glucose intolerance, and type 2 diabetes. Family studies have indicated a genetic susceptibility to PCOS. The aims of this study were 1) to assess glucose tolerance status, gonadotropins, and androgens in first degree relatives of patients with PCOS; and 2) to assess IR in normal glucose tolerant (NGT) family members. One hundred two family members of 52 patients with PCOS [Mothers(PCOS) (n = 34; mean age, 46.5 yr; mean body mass index (BMI), 28.8 kg/m(2)), Fathers(PCOS) (n = 24; mean age, 50.4 yr; mean BMI, 27.5 kg/m(2)), Sisters(PCOS) (n = 19; mean age, 25.1 yr; mean BMI, 22.9 kg/m(2)), and Brothers(PCOS) (n = 25; mean age, 23.7 yr; mean BMI, 22.5 kg/m(2))] and 82 unrelated healthy control subjects without a family history of diabetes or PCOS (4 age- and weight-matched subgroups, i.e. Control(MothersPCOS), Control(FathersPCOS), Control(SistersPCOS), and Control(BrothersPCOS)) were studied. Glucose and insulin (at baseline and during a 75-g, 2-h oral glucose tolerance test) were measured. IR was assessed by fasting insulin (FI), fasting glucose to insulin ratio (FGI), homeostatic model assessment (HOMA IR), and area under the curve for insulin during the oral glucose tolerance test (AUC(insulin)) in NGT Mothers(PCOS), Fathers(PCOS), Sisters(PCOS), Brothers(PCOS), and matched control subgroups. Including the prestudy-diagnosed 3 mothers and 2 fathers with diabetes, diabetes and impaired glucose tolerance (IGT) were noted in 16% and 30% of Mothers(PCOS) and 27% and 31% of Fathers(PCOS), respectively. There was no diabetes in Sisters(PCOS) and Brothers(PCOS). IGT was found in 5% of Sisters(PCOS). Impaired fasting glucose was found in 3% of Mothers(PCOS) and 4% of Brothers(PCOS). The analysis of NGT family members showed that Mothers(PCOS) had higher FI (P < 0.05), HOMA IR (P < 0.05), and AUC(insulin) (P < 0.01) and lower FGI (P < 0.05) than Control(MothersPCOS), whereas all IR parameters were comparable between Fathers(PCOS) and their matched control subgroup. Sisters(PCOS) had higher FI (P < 0.05), HOMA IR (P < 0.01), and AUC(insulin) (P < 0.05) and lower FGI (P < 0.01), and Brothers(PCOS) had higher AUC(insulin) (P < 0.01) than their matched control subgroups, respectively. Mothers(PCOS) had higher testosterone levels than Control(MothersPCOS) (P < 0.01 and P < 0.05 for pre- and postmenopausal women, respectively). Sisters(PCOS) had higher LH (P < 0.01), testosterone (P < 0.001), androstenedione (P < 0.01), and dehydroepiandrosterone sulfate (P < 0.05) levels than Control(SistersPCOS). There was no difference in gonadotropin and androgen levels in Fathers(PCOS) compared with Control(FathersPCOS) or in Brothers(PCOS) compared with Control(BrothersPCOS). Our results suggest that 1) first degree relatives of patients with PCOS may be at high risk for diabetes and glucose intolerance; 2) NGT female family members have insulin resistance; and 3) mothers and sisters of PCOS patients have higher androgen levels than control subjects. We propose that the high risks of these impairments warrant screening in first degree relatives of patients with PCOS.

Adult↗
PubMedDate not supplied

Glucose intolerance in uremia (A- and B-cell function during conservative and dialytic management.

Glucose tolerance and insulin and glucagon secretion were investigated in two groups of uremic patients, respectively on conservative and hemodialytic treatment. For this purpose, a glucose infusion was performed in the fasting state. Glucose intolerance was observed in uremic patients; hemodialysis improved, but did not normalize the glucose disposal. In uremic patients both on conservative and dialytic treatment plasma insulin and glucagon levels were higher than in the control group; the pattern of glucagon suppression was well maintained. The data obtained suggest that glucose intolerance in uremia is related mainly to peripheral insulin resistance and is not due to hyperglucagonemia.

Adult↗
PubMed2001

Amniotic fluid insulin at 14-20 weeks' gestation: association with later maternal glucose intolerance and birth macrosomia.

OBJECTIVE: To examine the hypothesis that early second trimester amniotic fluid (AF) insulin concentration is elevated and later fetal growth is augmented in gravidas demonstrating later oral glucose intolerance. RESEARCH DESIGN AND METHODS: In this prospective observational cohort study, AF was sampled at 14-20 weeks' gestation in 247 subjects, and 1-h 50-g oral glucose challenge tests (GCTs) were performed at > or = 24 weeks. AF insulin was assayed by an automated immuno-chemiluminometric assay (8). Macrosomia was defined as birth weight above the 90th centile. RESULTS: AF insulin concentration (range 1.4-44.5 pmol/l) correlated positively with gestational age and maternal weight. A logistic regression analysis, adjusted for maternal age and midpregnancy weight, showed increased AF insulin multiples of gestational age-specific medians to be associated with subsequently diagnosed gestational diabetes mellitus (GDM) (OR 1.9, CI 1.3-2.4, P = 0.029). Among 60 subjects with GCT values > 7.2 mmol/l, each unit increase in AF insulin multiple of median (MOM) was associated with a threefold increase in fetal macrosomia incidence (3.1, 1.3-4.9, P = 0.048). CONCLUSIONS: An elevated AF insulin concentration at 14-20 weeks' gestation is associated with subsequently documented maternal glucose intolerance. Among gravidas with GCT values > 7.2 mmol/l, elevated early AF insulin concentration is associated with fetal macrosomia. Maternal glucose intolerance may affect fetal insulin production before 20 weeks' gestation.

Amniocentesis↗
PubMed1999

Rehydration of moderately dehydrated children with transient glucose intolerance using rice oral rehydration solution.

Following the successful rehydration of two moderately dehydrated patients with transient glucose intolerance (TGI) using rice-oral rehydration solution (R-ORS), R-ORS has been used in Hacettepe University Ihsan Dogramaci Children's Hospital Diarrhea Training and Treatment Unit (DTTU) to rehydrate moderately dehydrated children with TGI. The files of children with moderate dehydration and glucose intolerance admitted to the unit were reviewed retrospectively within two periods according to the availability of R-ORS. The clinical and laboratory findings were analysed where available. Before R-ORS became available (September 1993) 6 patients were admitted, all of whom deteriorated with glucose (G)-ORS treatment in 7.0 +/- 3.8 h and were hospitalized for i.v. fluid treatment. During the second period 22 moderately dehydrated children with TGI were admitted. The clinical and laboratory characteristics on admission of the children in the two periods were not statistically different (p > 0.05). Among the 22 patients admitted during the second period 10 were administered G-ORS in the unit and 12 had already received G-ORS at home. Clinical and laboratory deterioration was observed in these 10 patients while receiving G-ORS in the unit within 6.3 +/- 3.7 h and rehydration was continued with R-ORS. Clinical and laboratory improvement were demonstrated in 8 patients within 18.2 +/- 6.5 h. Overall, 17 patients were rehydrated successfully with R-ORS, with a mean time of 18.0 +/- 7.2 h. Five patients were hospitalized. The overall success rate of R-ORS was 77.3%. R-ORS may be considered as an alternative mode of therapy to i.v. treatment in the rehydration of moderately dehydrated children with TGI.

Dehydration↗
PubMed2001

Prevalence and determinants of diabetes mellitus and glucose intolerance in a Canarian Caucasian population - comparison of the 1997 ADA and the 1985 WHO criteria. The Guía Study.

AIMS: To estimate the prevalence of diabetes mellitus, impaired fasting glucose and impaired glucose tolerance in a Canarian population according to the 1997 ADA and the 1985 WHO criteria; and to study the cardiovascular risk factors associated with these categories. METHODS: A total of 691 subjects over 30 years old were chosen in a random sampling of the population (stratified by age and sex). An oral glucose tolerance test was performed (excluding known diabetic patients) and lipids were determined in the fasting state. Anthropometric and blood pressure measurements were performed, and history of smoking habits and medications was recorded. RESULTS: The prevalence of diabetes was 15.9% (1997 ADA) and 18.7% (1985 WHO); the prevalence of impaired fasting glucose and impaired glucose tolerance was 8.8 and 17.1%, respectively. The age-adjusted prevalence of diabetes (Segi's standard world population) for the population aged 30-64 years was 12.4% (1985 WHO). The risk factors significantly associated with diabetes (1997 ADA and 1985 WHO) were age, body mass index; waist-to-hip ratio, systolic and mean blood pressure, triglycerides, total cholesterol and low HDL-cholesterol. Age, body mass index and systolic blood pressure were associated with impaired fasting glucose and impaired glucose tolerance; triglycerides were also associated with impaired fasting glucose. CONCLUSIONS: The prevalence of diabetes mellitus and glucose intolerance in Guía is one of the highest among studied Caucasian populations. The new 1997 ADA criteria estimate a lower prevalence of diabetes. Impaired fasting glucose also had a lower prevalence than impaired glucose intolerance and the overlap of these categories was modest.

Adult↗
PubMed2002

Sulfonylurea receptor knockout causes glucose intolerance in mice that is not alleviated by concomitant somatostatin subtype receptor 5 knockout.

OBJECTIVE: To examine the long-term effects of Sur KO, SSTR5 KO, and double Sur/SSTR5 KO on insulin secretion and glucose regulation. SUMMARY BACKGROUND DATA: The sulfonylurea receptor (Sur) and somatostatin receptor type 5 (SSTR5) play an integral role in the regulatory pathways of the endocrine pancreas. Sur knockout (KO) and SSTR5 KO mice were generated in the authors' laboratories and crossbred to generate Sur/SSTR5 KO mice. All mice were genotyped by Southern blotting and polymerase chain reaction analysis. METHODS: One-year-old Sur KO, Sur/SSTR5 KO, SSTR5 KO, and age-matched wild-type control mice underwent single-pass perfusion of isolated pancreata with low and high glucose concentration (n = 4-6/group). Another group of mice also underwent intraperitoneal glucose tolerance tests with 1.2 g glucose/kg body weight (n = 4/group per time point). RESULTS: Sur1 KO and Sur/SSTR5 KO mice had profoundly decreased insulin secretion in vitro, whereas SSTR5 KO had increased insulin secretion compared with wild-type mice. Sur1 KO and Sur/SSTR5 mice had increased glucose response in vivo compared with wild-type mice. Sur1 KO and Sur/SSTR5 KO mice exhibit glucose intolerance and SSTR5 KO mice show increased insulin response in vitro. CONCLUSIONS: Sur1 KO causes glucose intolerance and SSTR5 KO causes increased insulin secretion. However, Sur/SSTR5 double ablation does not alleviate the diabetic state of the Sur1 KO.

ATP-Binding Cassette Transporters↗
PubMed2001

Thyroid hormone excess and glucose intolerance.

The elevated plasma glucose levels in hyperthyroidism may be explained by increased rates of endogenous glucose production, due mainly to increased gluconeogenesis. The rates of insulin-stimulated glucose disposal in peripheral tissues in hyperthyroidism have been found, in general, either normal or increased. Skeletal muscle is the most important tissue for the disposal of glucose in response to insulin. In this tissue, insulin increases glucose disposal by stimulating glucose transport, glucose phosphorylation/glycolysis, glycogen synthesis and glucose oxidation. Studies examining insulin-stimulated glucose metabolism in skeletal muscle have suggested that, in the hyperthyroid state, it may be of primary importance to increase the rates of glycolysis and lactate formation relative to glucose oxidation in this tissue in order to provide substrate for gluconeogenesis (increase Cori cycle activity). This effect will be achieved primarily by a decrease in glycogen synthesis and an increase in glycogenolysis. When hyperthyroidism becomes more severe, an increased rate of glucose uptake into muscle may then be necessary since the increased conversion of glycogen to lactate could not be sustained for prolonged periods and might lead to a depletion in glycogen stores. This mechanism would ensure that the level of glucose in plasma is kept normal or slightly increased. Thus, an increased Cori cycle activity may be a necessary mechanism to provide optimal conditions in hyperthyroidism for the control of glucose utilization without increasing the risk of hypoglycemia. In addition to lactate, increased rates of gluconeogenesis in hyperthyroidism can also be sustained by increased plasma concentrations of amino acids (mostly glutamine and alanine) and glycerol, as well as by increased plasma concentrations of free fatty acids.

Animals↗
PubMed1984

The physiological significance of the glucose intolerance of aging.

Aging is associated with glucose intolerance, but its significance is unclear. We performed oral glucose tolerance tests and more physiologic meal tolerance tests in a group of 23 young adults, mean (+/- SE) age, 37 +/- 2 years and 17 elderly adults, mean age 69 +/- 1 years. The total glucose and insulin responses following the oral glucose load were increased by 24% and 127% respectively in the elderly compared with the young (24,524 +/- 1,080 vs. 19,734 +/- 702 mg/dl X min and 24,289 +/- 3,401 vs. 10,700 +/- 1,209 microU/ml X min). Following mixed meals, the total glucose response was 45,795 +/- 1,343 mg/dl X min in the young, compared with 50,998 +/- 1,850 mg/dl X min in the elderly (p less than .05) an 11% increase. Total insulin response was increased by 40% in the elderly (38,590 +/- 3,662 microU/ml X min) compared with the young (27,481 +/- 2,805 microU/ml X min) (p less than .05). We conclude that following the ingestion of more physiologic mixed meals, modest postprandial hyperglycemia and hyperinsulinemia can be demonstrated in elderly adults.

Adult↗
PubMed2000

Oral administration of branched chain amino acids improves virus-induced glucose intolerance in mice.

We investigated the therapeutic effect of branched chain amino acids (BCAA) on mice with glucose intolerance induced by encephalomyocarditis virus (EMCV). Male DBA/2 mice were divided into three groups: treated with BCAA, (such as valine, leucine, and isoleucine), untreated, and control. BCAA-treated and -untreated groups were inoculated intraperitoneally with the NDK25 variant of EMCV at 200 plaque-forming units per mouse. The BCAA-treated group was administered orally 0.9 g/kg/day of each BCAA from the day after viral inoculation. The control group neither received virus inoculation nor was treated with BCAA. One week after inoculation, oral glucose tolerance tests (OGTT) were performed. After the glucose loading at 1.5 g/kg of body weight, blood glucose levels in the untreated group were 92.0+/-10.0 mg/dl at baseline, 224.6+/-10.9 mg/dl at 30 min, and 169.4+/-21.4 mg/dl at 60 min, which were significantly (P<0.05) higher than those in the control group (62. 7+/-3.6 mg/dl, 167.2+/-16.4, and 83.8+/-6.0 mg/dl, respectively). Blood glucose levels in the BCAA-treated group were 54.5+/-3.7 mg/dl at baseline, 145.2+/-8.7 mg/dl at 30 min, and 128.7+/-18.3 mg/dl at 60 min after the glucose loading, which were not significantly higher than those in the control group. Immunoreactive insulin levels at 30 min after the glucose loading were lower in the untreated group than in the control group at 1 week after virus inoculation. Histological investigations showed that the grade of insulitis in the pancreas of mice of the BCAA-treated group was lower than that of the mice of the untreated group. These results suggest that oral administration of BCAA is able to improve glucose intolerance induced by EMCV.

Administration, Oral↗
PubMed2003

Dietary diacylglycerol-rich oil stimulation of glucose intolerance in genetically obese rats.

The effects of dietary 1,3-diacylglycerol-rich oil (DG oil) on glucose and lipid metabolism were investigated in comparison with triacylglycerol (TG) oil in female genetically obese Wistar fatty rats. The obese rats and their lean littermates (8 wk old) were fed a synthetic diet containing 10%, (w/w) DG or TG oil for 5 wk. The body weights, abdominal fat weights, and the plasma and liver TG concentrations were not significantly different due to dietary fat type in the obese and lean rats. The plasma glucose concentrations were significantly elevated by dietary DG oil as compared to TG oil in the portal vein and inferior vena cava of obese and lean rats. The plasma free fatty acid concentrations were markedly elevated by dietary DG oil as compared to TG oil in the portal vein and inferior vena cava of both genotype rats, particularly in the obese rats. In the glucose tolerance test, the obese rats fed DG oil showed glucose intolerance, possibly due to the markedly elevated plasma free fatty acids. Thus, the effects of dietary DG oil on lipid-lowering effects and anti-obesity were not observed in either genotype in the present study. Moreover, it is remarkable that glucose intolerance was induced by dietary DG oil in the genetically obese rats. dietary

Analysis of Variance↗
PubMed2002

Glucose intolerance induced by a high-fat/low-carbohydrate diet in rats effects of nonesterified fatty acids.

We examined the time course of effects of a high-fat/low-carbohydrate (HF/LC) diet on the impairment of glucose tolerance in rats, clarified whether insulin secretion and sensitivity were impaired by the HF/LC diet, and investigated the relationship between the increased nonesterified fatty acids (NEFA) after HF/LC diet feeding and insulin secretion and sensitivity. We found that glucose tolerance and the postglucose-loading insulin secretion were impaired after 3 and 7 d on the HF/LC diet. The glucose intolerance was accompanied by a rise in the fasting plasma NEFA level. When stimulated with 15 mmol/L of glucose, the insulin secretion was impaired in pancreatic islets from rats fed the HF/LC diet. Rats fed the HF/LC diet showed insulin resistance in vivo. The glucose-stimulated insulin secretion was inhibited in the islets following 24-h culture with palmitic acid. The 24-h infusion of palmitic acid decreased whole-body insulin sensitivity. In summary, at least 3 d on a HF/LC diet is needed to induce glucose intolerance in rats, and the impairment may be induced by decreased insulin secretion and sensitivity, which is related to the increase in the plasma NEFA level.

Animals↗
PubMedDate not supplied

Alterations in plasma lipids in the presence of mild glucose intolerance in the offspring of two type II diabetic parents.

Plasma lipids and oral glucose tolerance were determined in 67 normal control subjects (age range 19-67 yr) and 150 individuals (17-69 yr) who were offspring of two type II diabetic parents. Age- and weight-adjusted analyses of covariance were performed for lipids and for glucose and insulin responses. For both men and women, the mean concentrations of total, low-density-, and high-density-lipoprotein-cholesterol and of triglycerides in the offspring with normal glucose tolerance (N = 109) were similar to respective controls. For offspring with abnormal glucose tolerance (N = 41), the mean levels of total cholesterol, LDL-cholesterol, and triglycerides were significantly elevated (P = 0.02 or less) in women but not in men. The mean HDL-cholesterol levels were 20% lower and LDL/HDL-cholesterol ratios 60% greater in women with abnormal glucose tolerance, whereas no significant differences existed for any of the lipid fractions in men, compared with respective controls. Both men and women with abnormal glucose tolerance had a comparable magnitude of hyperglycemia as well as hyperinsulinemia. These observations indicate that significant alterations in plasma lipids exist in individuals with mild, asymptomatic glucose intolerance and there are important sex differences in lipid metabolism in the early stage of diabetes, despite comparable degrees of glucose intolerance and insulin responses.

Adolescent↗
PubMed1986

Immunohistochemical morphometry of pancreatic endocrine cells in diabetic, normoglycaemic glucose-intolerant and normal cats.

The anatomical distribution and volume fractions of pancreatic A cells (glucagon), B cells (insulin) and D cells (somatostatin) were evaluated by an immunoperoxidase technique in 6 diabetic cats, 6 normoglycaemic glucose-intolerant cats and 6 normal control cats. Islets lacking A cells were observed in some sections from the right lobe of the pancreas which correlated with a significantly lower A cell volume fraction in the right pancreatic lobe. Endocrine cell volume fractions in normoglycaemic glucose-intolerant cats were not significantly different from controls. Thus, a reduction in B cell volume fraction was not necessary for the occurrence of impaired glucose tolerance in these cats. However, the reduction of B cell volume fraction in the 2 normoglycaemic glucose-intolerant cats with insular amyloidosis may in part explain the more severely impaired glucose tolerance previously observed in these cats. Insular amyloidosis in our feline diabetics, as in human type II diabetics, was associated with a significant decrease in A and B cell volume fractions. In both human type II and feline diabetes mellitus, however, the reduction in B cell mass does not appear sufficient alone to lead to diabetes mellitus. Therefore, amyloid replacement of functional endocrine cells does not appear to be the primary diabetogenic event in feline diabetes mellitus, but may contribute to progression of the condition due to loss of functional B cell reserves. We thus postulate that a B cell defect precedes deposition of islet amyloid and that these amyloid deposits may thus provide an important biochemical clue to specific B cell derangements occurring in adult-onset diabetics.

Amyloidosis↗