[Glucose and insulin in glucose homeostasis in the liver].
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Biomedical subjects
Publications and source records attributed to S Halimi.
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Many studies have shown that zinc deficiency could decrease the response to insulin. In genetically diabetic animals, a low zinc status has been observed contrary to induced diabetic animals. The zinc status of human patients depends on the type of diabetes and the age. Zinc supplementation seems to have beneficial effects on glucose homeostasis. However, the mechanism of insulin resistance secondary to zinc depletion is yet unclear. More studies are therefore necessary to document better zinc metabolism in diabetes mellitus, and the antioxidant activity of zinc on the insulin receptor and the glucose transporter.
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The present knowledge about zinc deficiency and insulin-sensitivity is not yet established. Using three groups of rats fed zinc-depleted diet (ZD) zinc adequate diets, either Pair Fed or ad libitum for a six weeks period, we measured the glucose turn over by the euglycaemic hyperinsulinaemic clamp technique coupled with tritiated glucose as tracer. The basal hepatic glucose production (HGP) and insulinaemia were lower in zinc-depleted rats. At a low rate of insulin infusion (0.6 mU/min/rat) the zinc-depleted rats did not show any difference in hepatic insulin sensitivity compared with the pair-fed animals. At high level of insulin rate (3 mU/min/rat; 9 mU/min/rat), the zinc-depleted rats exhibited a lower glucose uptake compared to the two control groups (Pair-fed and Ad libitum animals). This peripheral insulin resistance is therefore related to a modification of insulin receptors, or post receptors events in zinc deficiency.
CA 19-9 is a monoclonal antibody-defined tumor marker expressed by exocrine pancreas. It has been shown that exocrine atrophy was associated with deficiency. Hyperamylasemia has been described during ketoacidosis. Our study aimed at investigating the relationships between CA 19-9 and metabolic control of diabetes. Study was performed on 51 adult consecutive diabetic patients (21 type 1 and 30 type 2), with ketoacidosis or hyperosmolarity (group A, n = 15), poor glycaemic control (group B, n = 19), or good control (group C, n = 17). Serum CA 19-9 and metabolic parameters were evaluated on day 1 and day 30. Analysis of variance showed a very significant global difference between groups for CA 19-9 (p less than 0.0001); group A (66.1 +/- 11.4 u/ml) significantly differed from group B (36.4 +/- 4 u/ml) (p less than 0.01) and group C (22.4 +/- 2.8 u/ml) (p less than 0.001). Simple regression showed a significant correlation between CA 19-9 and fasting blood glucose (r = 0.6, p less than 0.001), plasma creatinine level (r = 0.37, p = 0.01), bicarbonate (r = 0.47, p = 0.001) and HbA 1c (r = 0.33, p = 0.032). The Ca 19-9 decrease on day 30 paralleled the improvement of glycaemic control. We conclude that CA 19-9 in diabetic patients is raised in acute metabolic situations and correlated very well with blood glucose concentration. A careful interpretation of this tumor marker assay is required when screening for pancreatic carcinoma among diabetic patients. CA 19-9 could be a useful and sensitive marker for the severity of exocrine damage and functional cellular disorders following metabolic disturbances in diabetes.
Conjunctival angioscopy is a non invasive way for visualization and quantitative evaluation of the microcirculation. Grading red blood cell aggregation is possible in vivo using Ditzel's four grades score. The two-dimensional organization of conjunctival microvessels allows morphometric quantification of microvascular density. The aim of our study was to evaluate the determinant factors of erythrocyte aggregation and the place of conjunctival angioscopy in the early detection of diabetic microangiopathy. Conjunctival parameters were red blood cell aggregation (Ditzel's score) and morphometric evaluation of capillary, venular and arteriolar density. Criteria of diabetic microangiopathy were microalbuminuria and retinal fluorescein angiogram. Both conjunctival angioscopy and retinal angiogram were scored independently. Results obtained in 30 type 1 diabetic patients, with multifactorial statistical analysis, show that red blood cell aggregation in vivo is an essential discriminant factor for diabetic retinopathy and nephropathy. This rheological phenomenon depends more on duration of diabetes (analysis of variance p = .0005, r = .65) and metabolic control than on albuminemia or fibrinogenemia such as in non-diabetic patients. Manual morphometric data confirmed vascular rarefaction associated with excessive red blood cell aggregation (beta = .50). These results suggest that grading red blood cell aggregation in vivo is an interesting tool for physiopathological and clinical studies of diabetic microangiopathy.
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