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Systematic oral glucose tolerance tests in patients due for operation for senile cataract revealed the presence of latent diabetes, undiagnosed by standard investigations, in 20% of cases. The proportion of diabetics in patients with cataract is abnormally high when compared to a population free from cataract (43% as against 16%), which is in favor of a diabetic condition being the cause of lens opacification. An H.G.P.O. is therefore justified in all patients over 50 years of age with cataracts, especially those that are bilateral and mainly cortical.
There has been only limited research investigating the possible association between raised haematocrit levels, glucose intolerance and type 2 diabetes. In the present study, we explored the association between high haematocrit levels and impaired glucose tolerance by performing oral glucose tolerance tests in 46 patients with chronic obstructive pulmonary disease and no previous history of diabetes mellitus or glucose intolerance. A glucose metabolism disorder was observed in 12 (26%) patients (type 2 diabetes in six patients and impaired glucose tolerance in a further six). There was a significant association between high haematocrit levels and the presence of a glucose metabolism disorder, which was independent of other risk factors. High haematocrit levels may be an independent risk factor for type 2 diabetes and impaired glucose tolerance.
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OBJECTIVE: To investigate relationship between glucose metabolic disorders and expression of insulin receptor (IR) and tyrosine protein kinase (TPK) in posthepatitic cirrhosis hepatocyte and HBV DNA expression in pancreatic cells. METHODS: To detect HBV DNA in paraffin-embedded pancreatic and hepatic tissues from 12 posthepatitic cirrhosis patients with positive serum HBV markers by using in situ hybridization (ISH) with a digoxigenin labelled probe. The amount of IR and TPK have been evaluated by immunohistochemical quantitative analysis using image analyzer in hepatocyte of 12 patients positive for HBV markers with posthepatitic cirrhosis in serum. Immunofluorescent histochemical double staining technique was used. HBsAg and IR were observed under confocal laser scanning microscope. RESULTS: Eleven of 12 cirrhosis patients? hepatocytes were HBV DNA positive, including 7 patients (7/7) with impaired glucose tolerance (IGT) and 4 patients (4/5) with normal glucose tolerance (NGT). Eight of 12 pancreatic cells were HBV DNA positive, including 7 patients (7/7) with IGT, but only one patient (1/5) with NGT-HBV DNA was found positive in pancreatic cells in significantly more subjects in IGT group than in NGT group (P less than 0.01).IR and TPK amount in hepatocyte of IGT was significantly less than that of NGT patients with posthepatitic cirrhosis (P less than 0.01). IR amount was closely related to the TPK in cirrhosis hepatocyte r=0.82597(P less than 0.01). HBV DNA was mainly localized in the nuclei of hepatocyte and pancreatic acinar and islet cells. Immunofluorescent histochemical double-staining showed that HBsAg was partly localized in the IR positive areas of hepatocytes and pancreatic islet cells. CONCLUSION: HBV can invade acinar cells of pancreas and islet cells, which might be a direct cause of insulin-dependent diabetes mellitus-like the disorder and insulin absence after HBV infection. Decrease of IR and TPK might be main cause of noninsulin-dependent diabetes mellitus-like disorder after having hepatitis or posthepatitic cirrhosis.
OBJECTIVE: To explore the pathogenesis of glucose metabolic disorder and insulin resistance in critically ill children under severe stress. METHODS: To test glucose, lactate, glucagon, insulin, c-peptide, cortisol levels in 50 critically ill children. While we measured 125I-insulin binding to erythrocytes of 13 critically ill children who had hyperglycemia and hyperinsulinemia. Glucose and lactate were measured biochemically. Insulin, c-peptide, cortisol and glucagon were determined by RIA. Erythrocytes insulin receptor was detected by insulin radioreceptor assay. RESULTS: Glucose, lactate, insulin, c-peptide, glucagon, cortisol, insulin/glucose, insulin/glucagon ratio in patients were higher than those in normal controls (P < 0.05). As compared with normal controls, the maximum 125I-insulin bound and insulin receptor number per cell were significantly lower (P < 0.01). But there was no difference of mean value in receptor affinity (P > 0.05). CONCLUSIONS: Hyperglycemia is common in critically ill children during stress, which may be attributed to hormones disturbance and tissure insulin resistance. Insulin receptor defect due to comprehensive factors was one of the important causes for insulin resistance. The blood glucose level can be used as an predicting index in ICU.
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Patients with chronic liver disease (CLD) may show an abnormal glucose tolerance test (GTT). On the other hand, it is debated whether diabetics may undergo abnormalities of liver function. The aim of our study was to see whether galactose tolerance test (GaTT) is a suitable complementary diagnostic tool in defining the glucose metabolism abnormalities characteristic of the two above mentioned clinical entities. Thirty-one patients with CLD, 16 adult diabetics and 12 healthy volunteers were considered. GTT with radioimmunoassay of plasmatic insulin (IRI) and oral GaTT were performed. CLD patients were divided into two groups: with IRI/glycemia greater than 0.4 or less than 0.4. On GaTT, galactosemia was significantly raised in CLD compared to diabetics and control. Further, a statistically significant difference was shown in the glycemic variations during GaTT between diabetics and both CLD groups. A significantly inverse ratio galactosemia/glycemia occurred during GaTT and showed a different pattern between diabetics and CLD patients with impaired insulin secretion. A careful study of galactosemia and glycemia variations during GaTT reliably defines the different patterns of glucose metabolism derangement in CLD with abnormal GTT and in diabetics.
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BACKGROUND: The relationships between selected steroids, SHBG, growth hormone, IGF-1, IGF BP-3 and indicators of glucose metabolism were studied in the group of 20 female patients (15-20 yrs) on long-term treatment with low prednisone doses (< 0.3 mg/kg/day) (baseline phase) and after adding 1000 mg of metformin per day for following 6 months to improve impaired glucose metabolism (control phase). METHODS AND RESULTS: Lower basal DHEAS and DHEA (DHEA/S) levels were found as compared with reference values. Only DHEAS level returned into the reference range after the treatment with metformin. Decrease of DHEA/S depended on the doses (DHEAS -0.7621, DHEA -0.7685). Positive correlations between DHEA/S and of the results insulin tolerance were found as at the baseline (+0.4452, resp. +0.4455) as well as in the control period after the metformin administration (+0.7549, resp. +0.6073). Testosterone (T) and dihydrotestosterone(DHT) values were within the reference range during the whole study. Due to very low SHBG levels higher free androgen index (FAI) was recorded in more than half of the patients. Significant relationships were revealed between former gonadal androgens and indicators of glucose metabolism deterioration at the control phase: T correlated: with fasting insulin (+0.6005), with HOMAIR (+0.5380), with insulin/glucose (+0.5261), with fasting glucose (+0.9268), with AUC glucose (+0.6792), FAI: with fasting insulin (+0.5560), with HOMAIR (+0.5269), with fasting glucose (+0.9025), with AUC glucose (+0.7143), DHT: with fasting C peptide (+0.7921), with AUC C peptide (+0.7143). SHBG correlated: with fasting glucose (-0.6519), and with AUC glucose (-0.5868). The tendency of GH to lower, and IGF-1, IGF BP-3 to higher values at the baseline changed at the control phase: fasting and AUC value of GH increased (signif.), while were IGF-1 (nonsignif.) and IGF BP-3 (signif.) levels decreased. Surprisingly, no correlation was observed between GH and parameters of glucose metabolism. Contrary to GH, baseline IGFBP-3 values correlated: with HOMAIR (+0.5002), with insulin/glucose (+0.4860). The same relationships were found between AUC IGF BP-3 (+0.5676, +0.5559), IGF-1 (HOMAIR only +0.5412), IGF-1/IGF BP-3 (+0.5059, +0.5716) and parameters of insulin sensitivity (HOMAIR, insulin/glucose) in the control period. For the first time negative correlations between IGF-1, IGF-1 AUC, IGF BP-3, IGF-1/IGF BP-3 and somatostatin blood levels were discovered at the control phase. CONCLUSIONS: The study brought a number of new information about the importance of the "non-classical" glucoregulatory hormones in impairment of glucose metabolism, during long-term administration of low prednisone doses. The results suggest, that without normalisation of low DHEA/S, SHBG and high FAI levels it would not be possible to correct glucose metabolism properly in patients with long-term glucocorticoid therapy.
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In patients with hyperlipaemia, serum paraoxonase activities were polymodally distributed with 75% individuals in the low activity mode. In the same patients the distribution of serum cholinesterase activities was unimodal, but asymmetrical. Patients with impaired glucose tolerance or non-insulin-dependent diabetes mellitus had slightly higher cholinesterase activities than patients with hyperlipaemia only.
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