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PubMed1989

Effects of very mild versus overt diabetes on vascular haemodynamics and barrier function in rats.

Rats injected i.p. with a single dose of nicotinamide (250 mg/kg) 15 min prior to i.v. injection of streptozotocin (65 mg/kg) develop a very mild form of diabetes characterized by slight elevations of plasma glucose, increased levels of HbA1, and reduced insulin secretion in response to an i.v. glucose tolerance test. These rats gain weight normally and they are not hyperphagic, glycosuric, or polyuric. The effects of this very mild form of diabetes vs overt streptozotocin diabetes of three months duration on regional vascular 131I-albumin clearance, blood flow (assessed by 15 microns 85Sr-microspheres), and renal filtration function were examined in male Sprague-Dawley rats. Plasma glucose levels of rats with mild diabetes were 7.4 +/- 0.9 (mean +/- SD) (mmol/l) vs 6.5 +/- 0.6 for control rats and 31.3 +/- 6.0 for overtly diabetic rats. HbA1 levels were increased 1.4 fold in mildly diabetic and 2.3 fold in overtly diabetic rats. Vascular clearance of 131I-albumin was markedly increased in ocular tissues (anterior uvea, retina, and choroid), sciatic nerve, aorta, new (subcutaneous) granulation tissue, and kidney of both diabetic groups, although increases in overtly diabetic rats exceeded those in the mildly diabetic group (2.2-4.6 times control animals vs 1.6-3.3 times, respectively). Likewise, both overt and very mild diabetes markedly increased glomerular filtration rate (approximately 1.8 times and 1.2 times control animals, respectively), urinary excretion of endogenous albumin (approximately 9 times and 4 times) and IgG (approximately 15 times and 4 times), as well as regional blood flow in the anterior uvea, choroid, and sciatic nerve. Increases in tissue sorbitol levels were much larger in overtly diabetic rats (generally 10-20 times control animals) than in mildly diabetic rats (1.5-3 times controls). myo-Inositol levels were significantly decreased only in lens and sciatic nerve of overtly diabetic rats. These observations indicate that even very mild diabetes is associated with vascular functional changes which develop more slowly than in overtly diabetic rats, but are disproportionately large (in view of the minimal increases in glycaemia and tissue polyol levels) compared to those in overtly diabetic rats.

Animals↗
PubMed1989

Albuminuria in type 2 (non-insulin-dependent) diabetes mellitus and impaired glucose tolerance in Pima Indians.

The prevalence of abnormal urinary albumin excretion, defined by a urine albumin to creatinine ratio greater than or equal to 30 mg/g (approximately equivalent to an albumin excretion rate of greater than or equal to 30 mg/24 h), was determined in 2728 Pima Indians aged greater than or equal to 15 years from the Gila River Indian Community in Arizona, a population with a high prevalence of Type 2 (non-insulin-dependent) diabetes mellitus. Excessive albumin excretion was present in 8% of subjects with normal glucose tolerance, 15% of those with impaired glucose tolerance, and 47% of subjects with diabetes. The intermediate prevalence of abnormal albuminuria in those with impaired glucose tolerance suggests that hyperglycaemia even at levels below those diagnostic of diabetes is associated with renal abnormalities in some subjects and that these abnormalities may precede the onset of diabetes. Abnormal albuminuria at levels not reliably detected by the usual dipstick methods was commonly observed in Pima Indians with diabetes, even those with diabetes of recent onset. Associations were found with age, duration of diabetes, level of glycaemia, blood pressure, and treatment with insulin.

Adult↗
PubMed1984

Insulin, glucagon, and somatostatin release from the prediabetic Chinese hamster.

Diabetes mellitus in the adult Chinese hamster is characterized by subnormal pancreatic insulin release in vitro, decreased insulin content, and lack of obesity. The cause of the islet B-cell failure is not clear. We measured insulin, glucagon, and somatostatin release from in vitro perfused pancreases of young (mean age 10 and 20 weeks), genetically diabetic animals (subline AC, mean plasma glucose 8.0 and 16.6 mmol/l, respectively). Compared to age- and sex-matched normal hamsters (subline M, mean plasma glucose 5.3 mmol/l), the younger diabetic animals had a significantly elevated mean plasma glucose level, but net in vitro pancreatic release of insulin, glucagon, and somatostatin was normal. Pancreatic content of insulin and glucagon was also not significantly different from normal. At age 20 weeks, when the plasma glucose of the diabetic animals was even more elevated, pancreatic content and release of insulin were significantly subnormal, whereas glucagon and somatostatin release were normal, and pancreatic content of glucagon was normal. In a similar group of young (mean age 10 weeks) diabetic animals, non-fasting plasma insulin levels were within the normal range, but the corresponding glucose levels were excessive in most of the animals (13 out of 19). In conclusion, 10-week-old diabetic hamsters show mild hyperglycaemia which cannot be accounted for directly by decreased pancreatic release in response to a glucose plus arginine stimulus in vitro. Decreased ability of the B cell to respond in vivo to hyperglycaemia or peripheral resistance to insulin may contribute to later B-cell failure in the older diabetic hamster.

Aging↗
PubMed1995

Caloric restriction in obese pre-diabetic rats prevents beta-cell depletion, loss of beta-cell GLUT 2 and glucose incompetence.

Pre-diabetic male Zucker diabetic fatty rats (ZDF) become diabetic between 8 and 10 weeks of age. At that time their beta cells exhibit high basal insulin secretion, absent insulin response to glucose and loss of GLUT 2 glucose transporter. Beta-cell volume, which is increased at the onset of non-insulin-dependent diabetes, declines precipitously by age 18 weeks. To determine if expression of this diabetic phenotype was dependent upon the increased food intake of these rats, they were diet-matched to lean littermates for 12 weeks beginning at 6 weeks of age. Untreated control ZDF rats received an unrestricted diet for 3 months. All of the controls became hyperglycaemic by 8 weeks of age, whereas all diet-matched rats remained euglycaemic throughout the 3 months, despite the fact that at 18 weeks of age their mean body weight equaled that of obese rats on an unrestricted diet. In the former rats glucose-stimulated insulin secretion was absent at 12 weeks of age and GLUT-2-positive beta cells had fallen below 30%. The volume fraction of their beta cells was 2.6 times normal at this age but by 18 weeks of age it had declined by 75%. Diet restriction for 3 months prevented the loss of glucose-stimulated insulin secretion and the reduction of beta-cell GLUT-2 and beta-cell volume fraction. However, neither the elevated basal insulin secretion nor the exaggerated arginine-stimulated insulin secretion of the obese rats was reversed or prevented by caloric restriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Prevention of type 2 (non-insulin-dependent) diabetes mellitus by diet and physical exercise. The 6-year Malmö feasibility study.

From a previously reported 5-year screening programme of 6,956 47-49-year-old Malmö males, a series of 41 subjects with early-stage Type 2 (non-insulin-dependent) diabetes mellitus and 181 subjects with impaired glucose tolerance were selected for prospective study and to test the feasibility aspect of long-term intervention with an emphasis on life-style changes. A 5-year protocol, including an initial 6-months (randomised) pilot study, consisting of dietary treatment and/or increase of physical activity or training with annual check-ups, was completed by 90% of subjects. Body weight was reduced by 2.3-3.7% among participants, whereas values increased by 0.5-1.7% in non-intervened subjects with impaired glucose tolerance and in normal control subjects (p less than 0.0001); maximal oxygen uptake (ml.min-1.kg-1) was increased by 10-14% vs decreased by 5-9%, respectively (p less than 0.0001). Glucose tolerance was normalized in greater than 50% of subjects with impaired glucose tolerance, the accumulated incidence of diabetes was 10.6%, and more than 50% of the diabetic patients were in remission after a mean follow-up of 6 years. Blood pressure, lipids, and hyperinsulinaemia were reduced and early insulin responsiveness to glucose loading preserved. Improvement in glucose tolerance was correlated to weight reduction (r = 0.19, p less than 0.02) and increased fitness (r = 0.22, p less than 0.02). Treatment was safe, and mortality was low (in fact 33% lower than in the remainder of the cohort).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1991

Studies on autoimmunity for initiation of beta-cell destruction. VIII. Pancreatic beta-cell dependent autoantibody to a 38 kilodalton protein precedes the clinical onset of diabetes in BB rats.

Autoantibody to a rat islet cell-protein of 38 kilodalton was detectable at around 30 days of age in the sera of diabetes-prone Biobreeding (DP-BB) rats by both immunoprecipitation and differential Western blotting methods. Anti-38 kilodalton islet cell autoantibody was not, however, observed in the sera from 5- to 20-day-old DP-BB rats. Over 90% of DP-BB rats in which the antibody was detected, eventually developed Type 1 (insulin-dependent) diabetes mellitus. The antibody disappeared within 2 weeks after diabetes onset. However, it was preserved in the sera of DP-BB rats which had been treated with silica to prevent insulitis. The anti-38 kilodalton islet cell autoantibody was not detected in sera from control Wistar Furth (WF) rats. The autoantibody also cross-reacted with a rat insulinoma (RINm5F) cell protein of 38 kilodalton, but did not react with protein from mouse fibroblast (L-929 cells), rat pituitary cells (GH3 cells), or normal rat lymphocytes. The production of the autoantibody appears to be pancreatic Beta-cell dependent, since the autoantibody disappears after almost complete depletion of Beta cells, but is consistently present as long as Beta cells remain. Identification of the Beta-cell dependent anti-38 kilodalton islet cell autoantibody, which cross-reacts with a rat insulinoma cell protein of 38 kilodalton and precedes the onset of Type 1 diabetes in BB rats, will be invaluable for study of the molecular nature of a target islet cell autoantigen associated with the induction of autoimmunity in DP-BB rats.

Animals↗
PubMed1996

Elevated serum levels of macrophage-derived cytokines precede and accompany the onset of IDDM.

To determine whether cytokines could have a role in the development of insulin-dependent diabetes mellitus (IDDM), we measured serum levels of cytokines derived from T helper 1 (interleukin-2 and interferon-gamma), T helper 2 (interleukin-4 and interleukin-10) lymphocytes and macrophages (tumour necrosis factor-alpha, interleukin-1 alpha and interleukin-1 beta) in patients before and after the onset of IDDM. Recently diagnosed IDDM patients had significantly higher levels of interleukin-2, interferon-gamma, tumour necrosis factor-alpha and interleukin-1 alpha than patients with either long-standing IDDM, non-insulin-dependent diabetes (NIDDM), Graves' disease, or control subjects (p < 0.05 for all). Compared with control subjects, patients with long-standing IDDM and those with NIDDM had higher interleukin-2 and tumour necrosis factor-alpha levels (p < 0.01 for all). Interleukin-4 and interleukin-10 were detectable in sera of patients with Graves' disease only, while interleukin-1 beta was not detectable in the serum of any control or test subject. To investigate whether high cytokine levels precede the onset of IDDM, we studied 28 non-diabetic identical co-twins of patients with IDDM, followed-up prospectively for up to 6 years after the diagnosis of the index. Levels of tumour necrosis factor-alpha and interleukin-1 alpha were elevated above the normal range more frequently in the eight twins who developed diabetes than in those 20 who did not (p < 0.005). Analysis of T helper 1 and T helper 2 profiles of the twin groups did not reveal a clear difference between prediabetic twins and twins remaining non-diabetic. These results support the notion that T helper 1 lymphocytes may play a role in the development of IDDM. This is associated with release of macrophage-derived cytokines, which is also a feature of the prediabetic period. The lack of evidence of a dominant T helper 1 profile of cytokine release before diabetes onset suggests that additional events, activating this arm of the cellular immune response, are required in the immediate prediabetic period.

Autoantibodies↗
PubMed1996

Fasting proinsulin and 2-h post-load glucose levels predict the conversion to NIDDM in subjects with impaired glucose tolerance: the Hoorn Study.

The aims of the present study were to observe the natural history of impaired glucose tolerance and to identify predictors for development of non-insulin-dependent diabetes mellitus (NIDDM). A survey of glucose tolerance was conducted in subjects aged 50-74 years, randomly selected from the registry of the middle-sized town of Hoorn in the Netherlands. Based on the mean values of two oral glucose tolerance tests subjects were classified in categories of glucose tolerance according to the World Health Organization criteria. All subjects with impaired glucose tolerance (n = 224) were invited to participate in the present study, in which 70% (n = 158) were subsequently enrolled. During follow-up subjects underwent a repeated paired oral glucose tolerance test. The mean follow-up time was 24 months (range 12-36 months). The cumulative incidence of NIDDM was 28.5% (95% confidence interval 15-42%). Age, sex, and anthropometric and metabolic characteristics at baseline were analysed simultaneously as potential predictors of conversion to NIDDM using multiple logistic regression. The initial 2-h post-load plasma glucose levels and the fasting proinsulin levels were significantly (p < 0.05) related to the incidence of NIDDM. Anthropometric characteristics, the 2-h post-load specific insulin levels and the fasting proinsulin/fasting insulin ratio were not related to the incidence of NIDDM. These results suggest that beta-cell dysfunction rather than insulin resistance plays the most important role in the future development of diabetes in a high-risk Caucasian population.

Aged↗
PubMed1992

Altered islet beta-cell function before the onset of type 1 (insulin-dependent) diabetes mellitus.

To define the glucose to insulin dose-response relationship before the onset of diabetes, we studied 22 non-diabetic co-twins of patients with Type 1 (insulin-dependent) diabetes mellitus and nine control subjects. All had intravenous glucose tests at 0.02, 0.1 and 0.5 g/kg and were followed-up prospectively for at least 6 years. Seven twins developed diabetes a mean of 7 months later; the remaining 15 are now unlikely to develop diabetes. The seven pre-diabetic twins had higher fasting insulin levels than control subjects (4.2 +/- 2.0 vs 1.8 +/- 1.8 nmol/l; p less than 0.05); but lower glucose clearance (1.0 +/- 0.5 vs 1.9 +/- 0.7 %/min; p less than 0.05), first phase insulin response at 0.5 g/kg (21.1 +/- 23.2 vs 143 +/- 50 nmol/l; p less than 0.0001), and total insulin responses at 0.1 g/kg (p less than 0.05) and 0.5 g/kg (p less than 0.00005). Using a curve-fitting programme, the normal glucose to insulin relationship was lost in prediabetic twins who had lower coefficient of determination (R2) than control subjects (p less than 0.01). In contrast, 15 low-risk twins and their nine control subjects had similar fasting glucose and insulin levels, glucose clearance, R2 and insulin secretory responses to different glucose loads. The positive predictive values of subnormal R2 and subnormal first phase insulin response were 67% and 58% respectively. These observations demonstrate an altered glucose to insulin dose-response relationship and loss of maximum insulin secretory response to glucose before the onset of Type 1 diabetes.

Adolescent↗
PubMed1992

Islet amyloid polypeptide plasma concentrations in individuals at increased risk of developing type 2 (non-insulin-dependent) diabetes mellitus.

To study whether abnormal secretion of islet amyloid polypeptide is involved in the development of insulin resistance and impaired insulin secretion in Type 2 (non-insulin-dependent) diabetes mellitus, we measured islet amyloid polypeptide concentrations in 56 first-degree relatives of Type 2 diabetic subjects and in 10 healthy control subjects. Fasting islet amyloid polypeptide concentrations were similar in control subjects, glucose-tolerant and glucose-intolerant relatives (8 +/- 1, 9 +/- 1 and 11 +/- 2 fmol/ml; p = NS). The area under the islet amyloid polypeptide curve measured during an oral glucose load was larger in glucose-intolerant relatives (115 +/- 13 fmol/ml) compared to glucose tolerant relatives and control subjects (88 +/- 3 and 79 +/- 12 fmol/ml; p less than 0.05). The insulin response during the oral glucose load was inversely correlated with the rate of glucose disposal measured during a euglycaemic hyperinsulinaemic clamp (r = -0.725; p less than 0.01), while no significant correlation was observed between the corresponding values for islet amyloid polypeptide and glucose disposal (r = -0.380; p = NS). Hypersecretion of islet amyloid polypeptide is observed in glucose-intolerant first-degree relatives of patients with Type 2 diabetes. Since these patients are characterized by insulin resistance and abnormal first-phase insulin secretion, the putative role of islet amyloid polypeptide in the development of these abnormalities remains to be established. It is however, unlikely that islet amyloid polypeptide is involved in the development of insulin resistance as insulin-resistant relatives with normal glucose-tolerance showed normal islet amyloid polypeptide concentrations.

Adult↗
PubMed1993

Quantitative phenotypic and functional analyses of islet immune cells before and after diabetes onset in the BB rat.

Inflammatory cells invading islets are thought to be mediators of islet destruction in spontaneous autoimmune diabetes mellitus. Thus methods were developed to isolate and characterize in situ islet inflammatory cells from 75-95-day-old prediabetic and diabetic BB rats. Islet inflammatory cells were structurally examined using single- and double-colour flow cytometry. Functional studies consisted of cytolytic assays using normal rat islet target cells and in situ islet or spleen effector cells. Structural data reveal natural killer cells to be the major cell population (70%) of total immune cells present in inflamed islets during prediabetes. At diabetes onset, the natural killer cell population remained at a high level (47%), but an increasing population of T cells (40%) was noted also. Analyses of T-cell subsets before and after diabetes onset revealed CD4+ T cells as predominant (50-55% of total T cells) with double-negative (CD4-CD8-) T cells (25-30%) and CD8+ T cells (15-20%) also present in significant quantities. Activated T cells accounted only for a minority of T cells (< 3%). Functional studies indicate that in situ islet-derived cytolytic effector cells are more potent killers (ten-fold) of normal islet target cells than are splenic effector cells. These data suggest that in situ islet inflammatory cells (a) can be quantitatively studied both structurally and functionally; (b) express structural phenotypes differing substantially from splenic mononuclear cell populations; (c) are considerably more cytolytic than splenic effectors; and (d) should prove informative in determining the most significant autoimmune functional events prior to and during islet beta-cell destruction.

Animals↗
PubMed1993

Quantification of human cytoplasmic islet-cell antibodies which cross-react with mouse pancreas: a follow-up study in type 1 (insulin-dependent) diabetic patients and in first-degree relatives.

We studied the heterogeneity of cytoplasmic islet-cell antibodies for cross-reaction with mouse pancreas in 31 recent-onset Type 1 (insulin-dependent) diabetic patients and 31 first-degree relatives with islet-cell autoantibodies detected on human pancreas. Only six Type 1 diabetic patients displayed islet-cell antibodies binding to human pancreas but not to mouse pancreas. Among 15 first-degree relatives displaying such antibodies which did not react with mouse pancreas, including one identical twin and one subject with polyglandular autoimmunity, none developed diabetes or even lost acute insulin response to intravenous glucose after 5 years of follow-up. By contrast, 14 of 20 (70%) of the Type 1 diabetic patients with islet-cell antibodies detected on human pancreas, and five first-degree relatives who progressed to a loss of acute insulin response to glucose and then to either Type 1 diabetes or glucose intolerance, also displayed antibodies reactive with mouse islets. Surprisingly, islet-cell antibodies were detectable on mouse pancreas but not on human pancreas in four Type 1 diabetic patients and in one relative who progressed to diabetes. In the five relatives who progressed to metabolic abnormalities, islet-cell antibody titres on mouse pancreas, quantified by the fluorescence intensity per islet at each serum dilution, progressively increased concomitantly with the loss of acute insulin response to glucose, whereas islet-cell antibody titres on human pancreas remained stable. The usefulness of such quantification was also validated by the fact that antibody titres on mouse pancreas were decreased after 3 months (p < 0.01) in recent-onset Type 1 diabetic patients, while titres on human pancreas were not.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Immunocytochemical localization of heat-shock protein 60-related protein in beta-cell secretory granules and its altered distribution in non-obese diabetic mice.

Immuno-electron microscopy technique was employed to investigate the cellular distribution of 60 kDa heat-shock protein (HSP60) in pancreatic Beta cells of control and non-obese diabetic mice. In thin sections prepared from control mice, antibody to mammalian HSP60 cross-reacted with protein(s) located to mitochondria and secretory granules. In particular, prominent binding of the antibody was seen to the insulin core of the mature insulin-secreting granules. In comparison, very little immunoreactivity was observed with immature secretory granules or with the Golgi apparatus. No binding to secretory granules or mitochondria was observed with normal mouse serum or with unrelated sera. On Western blots, HSP60 antibody specifically interacted with a single 62 kDa islet cell protein. These results suggest the existence of an HSP60-related protein with a novel location in mature secretory granules of Beta cells. The preferential association of the HSP60-related protein with the insulin core was gradually lost in Beta cells of pre-diabetic non-obese diabetic mice, and correlated with the progression of insulitis. The decrease in the granular binding of the HSP60 antibody was accompanied by an increase in cytoplasm staining, and was concomitant with a significant expansion of the insulin core diameter. The altered distribution of the HSP60-related protein in prediabetic mice, together with our observation that immature secretory granules accumulate in these animals indicate that the presence of HSP60-related protein in secretory granules might be associated with the secretory function of Beta cells.

Aging↗
PubMed1992

Long-term suppression of postprandial hyperglycaemia with acarbose retards the development of neuropathies in the BB/W-rat.

The effect of the alpha-glucosidase inhibitor acarbose on postprandial hyperglycaemia was explored in the spontaneously diabetic BB/W-rat. Acarbose-treatment (5 mg.kg body weight-1.day-1) of diabetic BB/W-rats maintained on small doses of insulin, was associated with a 40% reduction in the 24-h glucose area compared to non-treated diabetic rats. Over a 4 month treatment period this reduction in cumulative hyperglycaemia resulted in a complete prevention of autonomic polyneuropathy as indicated by R-BAR values. The development of somatic polyneuropathy in the BB/W-rat was significantly attenuated by acarbose treatment with a partial prevention of the characteristic nerve conduction velocity slowing during the first 3 months of diabetes, but no longer at 4 months. Characteristic structural abnormalities associated with diabetes in this model, such as axonal atrophy and axo-glial dysjunction, were significantly but only partially prevented in rats treated with acarbose for a diabetes duration of 4 months. These data suggest that postprandial lowering of hyperglycaemia resulting in a decrease in cumulative hyperglycaemia retards the development of diabetic polyneuropathies in the BB/W-rat.

Acarbose↗
PubMed1991

Hyperinsulinaemia in obesity is not accompanied by an increase in serum proinsulin/insulin ratio in groups of human subjects with and without glucose intolerance.

Serum proinsulin is disproportionately elevated compared to insulin in Type 2 (non-insulin-dependent) diabetes mellitus. We studied the effect of obesity on serum proinsulin with varying degrees of glucose intolerance. Serum proinsulin and insulin were measured during a 75 g oral glucose tolerance test in 73 obese and 74 non-obese subjects with normal, borderline or diabetic-type glucose tolerance. Proinsulin was assayed by a direct radioimmunoassay using proinsulin-specific antiserum. Fasting serum proinsulin and insulin and the summed values of proinsulin and insulin during oral glucose tolerance test were significantly, or tended to be, higher in obese subjects than in those without obesity in each category of glucose tolerance. However, the molar ratio of proinsulin to insulin was nearly the same between obese and non-obese groups with a similar degree of glucose tolerance. On the other hand, the proinsulin/insulin ratio increased progressively with the deterioration of glucose tolerance. We conclude that proinsulin secretion is disproportionately increased in the presence of glucose intolerance but not by obesity itself. Each Beta cell seems to function normally in obese subjects while glucose tolerance remains normal.

Blood Glucose↗
PubMed1995

Hearing impairment in WBN/Kob rats with spontaneous diabetes mellitus.

The inner ear of spontaneously diabetic WBN/Kob rats was functionally and morphologically examined in order to elucidate the relationship between diabetes mellitus and hearing impairment. At 3 months of age, WBN/Kob rats were non-diabetic, and their hearing function was normal. At 6-7 months of age, they showed decreased glucose tolerance and an increasing tendency toward urinary excretion of glucose without high plasma concentration of glucose, and were therefore judged to be pre-diabetic. They also displayed a significant elevation of hearing threshold in the auditory brainstem response, but showed little morphological and histochemical changes in the inner ear. At 12-13 months of age, they were spontaneously diabetic and showed a more apparent elevation of hearing threshold in auditory brainstem response than that in pre-diabetic animals. In addition, they displayed a marked decrease in the number of spiral ganglion cells and oedematous changes in the stria vascularis. The stria vascularis also showed a decrease in the intensity of staining with some lectins, i.e., wheat germ agglutinin, succinylated wheat germ agglutinin, Soranum tuberosum lectin, and concanavalin A. In conclusion, hearing impairment is induced by diabetes in the WBN/Kob rats first as an elevation of hearing threshold along with glucose intolerance; secondly, as a decrease in the number of spiral ganglion cells; and thirdly, as oedematous change of the stria vascularis with decreased intensity of lectin staining.

Aging↗