Zinc supplementation improves glucose disposal in patients with cirrhosis (original) (raw)
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TURKISH JOURNAL …, 2002
To investigate the effect of low dietary zinc intake and experimental diabetes (IDDM) on the zinc and carbohydrate metabolism, 8-week-old male wealing normal albino (Wistar) rats were fed diets containing either adequate (54mg/kg) or low zinc (1mg/kg) quantities for one week. Ten rats from each group (n=20) were then intraperitoneally injected with alloxan to induce diabetes. The rats were sacrificed after a further three weeks. Body weight gain and food intake were recorded regularly. On day 28, after an overnight fast, the animals were sacrificed and blood glucose, serum insulin, serum cholesterol concentrations, liver glycogen contents, and femur and pancreatic zinc concentrations were determined. Diabetic rats fed a low zinc or control diet had a low body weight gain, high total food intake (hyperphagia), low serum insulin, low liver glycogen contents and high serum cholesterol concentrations compared to normal rats. The consumption of the low zinc diet had only a minimal effect on the zinc status of rats as indicated by the growth rate, food intake and femur and pancreatic zinc concentrations. However, both diabetic and non-diabetic rats fed a low zinc diet had higher blood glucose than their control counterparts. Liver glycogen was also found to be higher in the low zinc non-diabetic rats than in their controls. Serum insulin and serum cholesterol concentrations were unaffected by dietary regimen. To conclude, the present study demonstrates that a reduced zinc intake had an effect on glucose utilization in both diabetic and non-diabetic rats and on glycogen deposition in non-diabetic rats. However, there were negligible changes in zinc status. Therefore, it appears that abnormalities in the carbohydrate metabolism may occur before tissue zinc depletion becomes apparent.
Interrelationships of zinc with glucose and insulin metabolism in humans
Biological Trace Element Research, 1990
Hyperzincemia has been reported to cause alterations in the homeostasis of glycid metabolism. To determine this effect on plasma glucose and insulin levels, we studied 36 normal individuals of both sexes aged 22–26 y after a 12-h fast. The tests were initiated at 7:00am when an antecubital vein was punctured and a device for infusion was installed and maintained with physiological saline. Zinc was administered orally at 8:00am. Subjects were divided into an experimental group of 22 individuals who received doses of 25, 37.5, and 50 mg of zinc and a control group of 14 individuals. Blood samples were collected over a period of 240 min after the basal samples (−30 and 0 min). We did not detect any change in plasma glucose or insulin levels, a fact that we attribute either to the ineffectiveness of the 50 mg dose of zinc or to the lack of human response to the acute action of this trace element. The individuals who ingested zinc showed a significant fall in plasma cortisol, probably caused by the action of this trace element.
Nutritional effects of oral zinc supplementation in cirrhosis
Nutrition Research, 2000
Poor zinc status is common in cirrhosis. Experimental studies proved that zinc supplementation produces metabolic effects, and trends towards improved liver function and nutritional status have previously been reported. We measured liver function by means of dynamic, quantitative tests and biochemical indices of nutrition in response to zinc treatment in patients with cirrhosis. Fifteen patients with advanced cirrhosis were studied before and after long-term oral zinc-sulfate supplementation (200 mg t.i.d, for 2-3 months). Liver function was measured by routine biochemistry, galactose elimination capacity and antipyrine clearance; nutritional assessment included the measurement of daily urinary creatinine excretion, and albumin, prealbumin, retinol-binding protein and insulinlike growth factor-1 (IGF-1) serum or plasma concentrations. In 10 patients data were correlated with the parameters of glucose metabolism obtained during a frequently-sampled i.v. glucose tolerance test. At baseline, serum zinc was low normal or reduced, and returned to normal range in all patients after supplementation. Liver function improved significantly. All nutritional indices improved as well, but remained on average below normal. IGF-1 increased on average by 30%, but was in the normal range in only 2 cases. Changes in IGF-1 correlated with improved glucose tolerance after i.v. glucose load, namely with the increased non-insulin-mediated glucose uptake. The study confirms that oral zinc produces metabolic effects in zinc-deficient patients with cirrhosis. Improved liver function and nutritional status may increase glucose disposal via increased IGF-1, responsible for the non-insulin-dependent fraction of glucose disappearance.
Biological Trace …, 2001
Diabetes mellitus is a group of metabolic disorders, the incidence of which varies widely throughout the world. The treatment of diabetes mellitus includes insulin, oral antidiabetic agents, and dietary regimens. Although the emphasis is on macronutrients intakes, there is strong evidence that there is an abnormal metabolism of several micronutrients in diabetic individuals. Zinc is one of the essential micronutrients of which status and metabolism is altered in this condition. This work is a short review about the close relation among zinc, glucose metabolism, and insulin physiology, as well as about the few experimental data about zinc absorption and zinc supplementation in diabetes mellitus patients.
Journal of Biochemical and Molecular Toxicology, 2020
Diabetes mellitus is a serious worldwide metabolic disease, which is accompanied by hyperglycaemia and affects all organs and body system. Zinc (Zn) is a basic cofactor for many enzymes, which also plays an important role in stabilising the structure of insulin. Liver is the most important target organ after pancreas in diabetic complications. In this study, we aimed to investigate the protective role of Zn in liver damage in streptozotocin (STZ)-induced diabetes mellitus. There are four experimental groups of female Swiss albino rats: group I: control; group II: control + ZnSO 4 ; group III: STZ-induced diabetic animals and group IV: STZ-diabetic + ZnSO 4. To induce diabetes, STZ was injected intraperitoneally (65 mg/kg). ZnSO 4 (100 mg/kg) was given daily to groups II and IV by gavage for 60 days. At the end of the experiment, rats were killed under anaesthesia and liver tissues were collected. In the diabetic group, hexose, hexosamine, fucose, sialic acid levels, arginase, adenosine deaminase, tissue factor activities and protein carbonyl levels increased, whereas catalase, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase, glutathione reductase and Na + /K +-ATPase activities decreased. The administration of Zn to the diabetic group reversed all the negative effects/activities. According to these results, we can suggest that Zn has a protective role against STZ-induced diabetic liver damage.
Biological Trace Element Research, 1992
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. Index Entries: Diabetes mellitus; zinc deficiency; insulin-resistance; antioxidant; insulin receptor; glucose transporter.
Diabetes and zinc dyshomeostasis: Can zinc supplementation mitigate diabetic complications?
Critical Reviews in Food Science and Nutrition, 2020
Zinc present in the islet cells of the pancreas is crucial for the synthesis, storage, and secretion of insulin. The excretion of large amounts of zinc from the body is reported in diabetic situations. Zinc depletion and increased oxidative stress have a major impact on the pathogenesis of diabetic complications. It would be most relevant to ascertain if intervention with supplemental zinc compensating for its depletion would beneficially mitigate hyperglycemia and the attendant metabolic abnormalities, and secondary complications in diabetes. An exhaustive literature search on this issue indicates: (1) Concurrent hypozincemia and decreased tissue zinc stores in diabetes as a result of its increased urinary excretion and/or decreased intestinal absorption, (2) Several recent experimental studies have documented that supplemental zinc has a potential hypoglycemic effect in the diabetic situation, and also beneficially modulate the attendant metabolic abnormalities and compromised antioxidant status, and (3) Supplemental zinc also alleviates renal lesions, cataract and the risk of cardiovascular disease accompanying diabetes mellitus, and help restore gastrointestinal health in experimental diabetes. These studies have also attempted to identify the precise mechanisms responsible for zinc-mediated beneficial effects in diabetic situation. The evidence discussed in this review highlights that supplemental zinc may significantly contribute to its clinical application in the management of diabetic hyperglycemia and related metabolic abnormalities, and in the alleviation of secondary complications resulting from diabetic oxidative stress.
Oral Zinc Supplementation Protects Rat Kidney Tissue from Oxidative Stress in Diabetic Rats
Kafkas Üniversitesi …, 2012
Zinc (Zn) is a trace element possessing a wide range of functions and antioxidant properties. This study was undertaken in order to illuminate the conflicting data on the status of zinc in diabetes, present in literature. Female Swiss albino rats were randomly divided into 4 groups: Group I, control; Group II, control + zinc sulfate; Group III, streptozotocin (STZ)-diabetic; Group IV, STZ-diabetic + zinc sulfate. Diabetes was induced by intraperitoneal injection of STZ (65 mg/kg body weight). Zinc sulfate was given daily by gavage at a dose of 100 mg/kg body weight every day for 60 days to Groups II and IV. At the last day of the experiment, rats were killed under anesthesia, kidney tissue was taken and homogenized. Antioxidant enzyme activities such as catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD) and myeloperoxidase (MPO), were determined in tissue homogenates as well as protein carbonyl content (PCC). Carbonic anhydrase (CA) was also determined as a functional enzyme for kidney. It was shown that kidney tissue antioxidant enzyme activities which were significantly impaired in the untreated diabetic group, were reversed in zinc treated diabetic groups, thus showing the beneficial effect of Zn treatment in diabetes via its antioxidant effect.
Biological Trace Element Research, 2019
Zinc (Zn) plays crucial roles in mammalian metabolism. There is increasing interest about the potential beneficial effects of Zn on the prevention or treatment of non-communicable diseases. This review critically analyzes the information related to the role of Zn on the metabolic syndrome (MetS) as well as type 2 diabetes (T2D), and summarizes the biological basis of these potential effects of Zn. There are several mechanisms by which Zn may help to prevent the development or progression of MetS and T2D, respectively. Zn is involved in both insulin secretion and action in peripheral tissues. Specifically, Zn has insulin-mimetic properties that increase the activity of the insulin signaling pathway. Zn modulates long-chain polyunsaturated fatty acids levels through its action on the absorption of essential fatty acids in the intestine and its subsequent desaturation. Zn is also involved in both the assembly of chylomicrons and lipoproteins as well as their clearance, and thus, plays a role in lipolysis regulation. Finally, Zn has been found to play a role in redox metabolism, and in turn, on blood pressure. The evidence related to the association between Zn status and occurrence of MetS is inconsistent. Although there are several studies reporting an inverse relationship between Zn status or dietary Zn intake and MetS prevalence, others found a direct relationship between Zn status and MetS prevalence. Intervention studies also provide confusing information about this issue, making it hard to reach firm conclusions. Zn as part of the treatment for patients with T2D has been shown to have positive responses in terms of glucose control outcomes, but only among those with Zn deficiency.