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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of Zn2+ in mimicking insulin in vivo and in vitro are further characterized. Like insulin, Zn2+ stimulated the conversion of [U-14C]-, [1-14C]-, and [6-14C]glucose to lipids in rat adipocytes. Maximum stimulation of lipogenesis was 55-80% of maximum insulin response after preincubation (30 min at 37 degrees C) of adipocytes with ZnCl2 (0.4 mM). Under these conditions, the half-maximum effect was achieved at 0.17 +/- 0.02 mM of ZnCl2. Similarly, an insulinlike effect of Zn2+ was observed on the oxidation of glucose by both pathways, glycolytic and hexose monophosphate shunt. In contrast, unlike insulin, Zn2+ did not inhibit lipolysis but rather exhibited a slight lipolytic activity. Also, the effect of Zn2+ on hexose influx did not exceed 14 +/- 3% that of insulin. The stimulatory effects of Zn2+ were not related to generation of H2O2. Catalase (100 micrograms/ml) did not inhibit Zn(2+)-stimulated glucose oxidation and its incorporation into lipids. Zn2+ had an additive effect on either insulin- or vanadate-stimulated conversion of [1-14C]glucose to fat, and together, the effect was approximately 140% of the maximum rate of lipogenesis. Chelation of intracellular Zn2+ by the cell-permeable chelator N,N,N',N'-tetrakis (2-pyridylmethyl)ethylenediamine did not significantly affect the ability of insulin to stimulate lipogenesis. Adipocytes derived from STZ rats were largely refractory to the modulating action of insulin. In contrast, the effect of Zn2+ on lipogenesis in these cells was more pronounced.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1992 Aug
PMID:Insulinlike effects of zinc ion in vitro and in vivo. Preferential effects on desensitized adipocytes and induction of normoglycemia in streptozocin-induced rats. 162 74

Zinc-calcium-phosphorous oxide (ZCAP) ceramics were developed to deliver insulin in vivo in rats. Thirty-nine Sprague-Dawley male albino rats (Holtzman Co., Madison, WI), weighing 260 +/- 15 g each, were randomly distributed into six groups: normal controls (3), sham controls (3), diabetic controls (6) and three diabetic experimental groups each consisting of nine rats. Diabetes was induced in rats by an intravenous injection of Streptozotocin (75 mg/kg body weight). Rats in the three diabetic experimental groups were implanted subcutaneously with two ZCAP capsules, each containing 10, 15, or 20 mg of insulin. Blood glucose measurements were taken at least twice a week over a six week period. Plasma insulin levels were measured at two, four, and six weeks by a radioimmunoassay using 125I labeled insulin. Normoglycemia was maintained for three weeks in rats implanted with ZCAP capsules containing a total of 20 mg of insulin. Plasma insulin levels correlated with the normal blood glucose levels in these rats. Thus, ZCAP capsules could be used to deliver insulin and maintain normoglycemia in diabetic rats.
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PMID:Insulin delivery by zinc calcium phosphate ceramics. 164 23

The relationship between renal hemodynamic abnormalities and renal kallikrein activity was studied in streptozocin-induced diabetic rats. Diabetic rats were either not treated with insulin and had plasma glucose levels greater than 400 mg/dl (severely hyperglycemic diabetic [SD]) or were treated with 1.5-1.75 U/day protamine zinc insulin and had glucose levels of 200-300 mg/dl (moderately hyperglycemic diabetic [MD]). In SD rats, kidney tissue level and excretion of active kallikrein were reduced after 3 wk compared with age-matched nondiabetic control rats (tissue, 11.7 +/- 1.9 vs. 20.5 +/- 1.8 ng/mg protein, P less than 0.005; urine, 126 +/- 12 vs. 179 +/- 10 micrograms/24 h, P less than 0.005). Despite increased kidney size, renal plasma flow (RPF) was reduced in SD rats (5.38 +/- 0.23 vs. 6.37 +/- 0.20 ml/min, P less than 0.05). Glomerular filtration rate (GFR) was not significantly lower (2.77 +/- 0.60 vs. 3.02 +/- 0.56 ml/min). In MD rats, kidney tissue level and excretion of active kallikrein were increased after 5 wk compared with age-matched nondiabetic control rats (tissue, 28.4 +/- 1.3 vs. 23.3 +/- 1.7 ng/mg protein, P less than 0.05; urine, 289 +/- 16 vs. 196 +/- 13 micrograms/24 h, P less than 0.001). In MD rats, GFR and RPF were increased (3.80 +/- 0.11 and 8.04 +/- 0.17 ml/min, respectively) compared with control rats (3.22 +/- 0.05 and 7.28 +/- 0.09 ml/min, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1990 Mar
PMID:Renal kallikrein and hemodynamic abnormalities of diabetic kidney. 168 83

Diabetic patients commonly have increased urinary excretion of zinc, although blood concentrations may be normal, lowered, or raised. We analyzed zinc levels in plasma and urine after an intravenous overload of zinc sulphate (8 mg) in 22 patients with insulin-dependent diabetes mellitus (IDDM) and 22 healthy individuals. No significant differences were found in basal levels of serum zinc in either group (111 +/- 29 micrograms/dl in IDDM vs 119 +/- 19 micrograms/dl in controls), although urinary excretion of zinc was significantly raised in diabetics (1396 +/- 622 micrograms/24 h) versus controls (611 +/- 235 micrograms/24 h). After zinc overload, both serum and urinary levels of this element varied between the two groups. Serum zinc in IDDM patients initially increased more markedly, and subsequently showed a more significant decline, than in controls. Urinary zinc levels in IDDM patients, in contrast to control values, showed no increase after overload. These alterations in serum and urinary zinc concentrations suggest that our diabetic patients may be zinc-deficient.
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PMID:Zinc levels after intravenous administration of zinc sulphate in insulin-dependent diabetes mellitus patients. 174 2

A 66-year old male with severe hyperglycaemia due to previously uncontrolled diabetes mellitus was also suffering from arteriosclerosis obliterans and diabetic nephropathy. The patient was treated with 16 IU/day insulin zinc suspension. In addition, an intravenous infusion of 80 micrograms/day prostaglandin E1 was given for 28 days in an attempt to improve the arteriosclerosis obliterans and diabetic nephropathy. Treatment resulted in a reduction in fasting blood glucose but no decline in urinary protein. Prostaglandin E1 treatment, however, produced an improvement in renal haemodynamics assessed by renography.
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PMID:Effect of prostaglandin E1 on renal haemodynamics in a patient with diabetic nephropathy. 177 11

Zinc is known to be an essential trace metal which is necessary for health and growth, and is also essential for the function and activity of over 200 metalloenzymes. A relationship between zinc and obesity was first found in obese patients and obese mice (genetically and dietary obese) to that the obese had lower blood zinc levels than their lean controls, and the zinc level was inversely related to the degree of obesity. The therapeutic effect of zinc on obesity is still a controversial subject. This study was to investigate the alterations of tissues zinc distribution, dietary zinc effect in obese mice, and the interactive combinations of zinc and endocrine factors in obese patients. Zinc and body fat contents were determined by atomic absorption spectrometer and gravimetrically, respectively. The results indicated that dietary zinc treatment increased body fat deposition in obese mice. Obese mice carried markedly low zinc levels in most of the peripheral tissues, but retained a great amount of zinc in liver and adipose tissues compared with lean mice. Clinically, zinc was found to be correlated with thyroid hormone conversion and insulin resistance. Although the true metabolic role of zinc in obesity is still obscure, the relationships between zinc, endocrine factors, and neurotransmitters, and interactions with other trace metals are needed to throw light on the subject. These approaches to thermoregulation and metabolic mechanisms of obesity and diabetes mellitus may be of great interest in the future.
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PMID:[Investigation of the relationships between zinc and obesity]. 179 13

The dynamics of changes of the Zn content in the pancreatic islets of rabbits after dithizon injection was studied. The amount of this metal in the islets reduced due to destruction of the cells and under the effect of high blood plasma glucose concentration. The insulin producing cells were devoid of zinc in diabetes of long duration with high hyperglycemia.
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PMID:[The dynamics of the Zn content in the pancreatic islets of rabbits after the administration of the diabetogenic agent dithizone]. 179 53

We report an unusual case of insulin allergy. A 48-year-old man with non-insulin-dependent diabetes mellitus receiving biosynthetic isophane human insulin (Humulin N) developed itchy wheal-and-flare reactions at the sites of injection. When Humulin N was changed to a semi-synthetic crystalline human insulin zinc (Novolin U), the allergic reactions completely disappeared. Evaluation of his serum showed a high level of insulin-specific IgE. Skin testing with all commercially available insulins showed immediate local reactions to all agents tested except for Novolin U. In addition, decrystallized Novolin U prepared by lowering the pH with acetic acid also induced a positive reaction. These observations suggest that the crystallized structure of human insulin may mask its antigenicity for allergic reactions.
Diabetes Res Clin Pract 1991 May
PMID:A case of insulin allergy: the crystalline human insulin may mask its antigenicity. 187 5

Diabetogenic and acidotropic effects of dithizone, 8-(p-toluenesulfonylamino)-quinoline and 8-(benzenesulfonylamino)-quinoline were studied in experiments on cats, rabbits, golden hamsters and mice. Selective damage of insulin producing cells, phase glycemic fluctuations and permanent diabetes development were shown to be connected with chelator zinc binding in the lysosome-segregation apparatus of these cells.
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PMID:The diabetogenic and acidotropic effects of chelators. 187 12

The involvement of Zn2+ in the inhibitory action of insulin and phenformin on bulk proteolysis was studied in the Langendorff rat heart with a Zn(2+)-buffering perfusate (0.1 mM citrate, physiological complete amino acids and 0.2% albumin). Proteins were biosynthetically labeled in vitro for 10 min with [3H]leucine. Rapidly degraded proteins were eliminated during a 3-h preliminary degradation without insulin or added Zn2+ (2 mM nonradioactive leucine). Insulin (5 nM), the lysosomal inhibitor chloroquine (30 microM), and the biguanide antihyperglycemic agent phenformin (2 microns) each caused a sustained 35-40% inhibition of [3H]leucine release beginning within 1-2 min and reaching a maximum at 1-1.5 h. When these agents were combined, their simultaneous proteolytic inhibitory effects were not appreciably greater than the effect of chloroquine alone. Infusion of supraphysiological perfusate Zn2+ (greater than 15 microM) mimicked the inhibitory effect of insulin and chloroquine on lysosomal proteolysis. Infusion of supraphysiological Co2+, Mn2+, Fe2+, and Cr3+ (30 microM, 0.5 h) caused no change in proteolysis; however, 30 microM Cu2+ caused a slight inhibition. Presumptive chelation of the background (approximately 20 nM) Zn2+ by infusion of 3 microM CaNa2 EDTA caused no change in protein degradation over 1-2 h. The infusion of a physiological concentration of 1 or 5 microM Zn2+ (as ZnCl2) caused no change in protein degradation over 1-2 h. Biguanides are known to reversibly form a Zn2+ complex with affinity less than that of Zn2+ for EDTA. Prior infusion of 3 microM CaNa2 EDTA inactivated the proteolytic inhibitory effect of maximal (2 microM) phenformin over at least 1.25 h of concurrent infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1991 May
PMID:Effect of Zn2+ on the proteolytic inhibitory action of insulin and biguanide antihyperglycemic drugs. 190 28


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