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Query: UMLS:C0011849 (diabetes)
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The effects of daily supplemental chromium (200 micrograms) complexed with 1.8 mg nicotinic acid on plasma glucose and lipids, including total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides, were assessed in 14 healthy adults and 5 adults with noninsulin-dependent diabetes mellitus (NIDDM) using a double-blind crossover study with 8-wk experimental periods. Eight of the 14 healthy subjects and all 5 subjects with NIDDM also underwent an oral glucose tolerance test with assessment of 90 min postprandial plasma glucose and insulin concentrations. No statistically significant effects of chromium nicotinic acid supplementation were found on plasma insulin, glucose, or lipid concentrations, although chromium nicotinic acid supplementation slightly lowered fasting plasma total and LDL cholesterol, triglycerides, and glucose concentrations, and 90-min postprandial glucose concentrations in individuals with NIDDM.
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PMID:Effect of chromium nicotinic acid supplementation on selected cardiovascular disease risk factors. 909 56

A possible new mechanism for the amplification of insulin receptor tyrosine kinase activity in response to insulin has been identified. The chromium-containing oligopeptide low molecular weight chromium-binding substance (LMWCr) does not effect the tyrosine protein kinase activity of rat adipocytic membrane fragments in the absence of insulin; however, insulin-stimulated kinase activity in the membrane fragments is increased up to 8-fold by the oligopeptide. Using isolated rat insulin receptor, LMWCr has been shown to bind to insulin-activated insulin receptor with a dissociation constant of circa 250 pM, resulting in the increase of its tyrosine protein kinase activity. The ability of LMWCr to stimulate insulin receptor tyrosine kinase activity is dependent on its chromium content. The results appear to explain the previously poorly understood relationship between chromium and adult-onset diabetes and cardiovascular disease.
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PMID:Chromium oligopeptide activates insulin receptor tyrosine kinase activity. 910 44

Transplantation of cells and organs from pigs to human beings offers potential treatment for medical conditions such as diabetes, kidney and heart failure, and Parkinson's disease. When the antibody-mediated hyperacute rejection barrier is overcome, a xenograft may not be treated as an allograft by the human immune system. Without prior culture with porcine cells, human lymphocytes are cytotoxic to some porcine cells. Our aim was to functionally characterize this direct cytotoxic response to porcine PHA-lymphoblasts and lymphocytes. Peripheral blood mononuclear cells from seven of eight human beings were cytotoxic to porcine PHA-lymphoblasts in bulk chromium-release assays, but not to the porcine lymphocytes from which the PHA-lymphoblasts were derived. The NK cell-sensitive cell line K562 only partly blocked the response to the PHA-lymphoblasts. IL-2-expanded clones of human lymphocytes were able to discriminate between PHA-lymphoblasts from two pigs and unable to lyse K562. When using IL-2 to make the anti-porcine cells proliferate under limiting dilution conditions, the proliferation and/or function of these cells did not conform to single-hit kinetics. All the observations from experiments with cells in bulk cultures and as short-term clones suggest that the direct cytotoxic response of human lymphocytes to porcine cells is heterogeneous and composed of a small population of in vivo-activated T cells as well as NK cells.
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PMID:Direct cytotoxic response of human lymphocytes to porcine PHA-lymphoblasts and lymphocytes. 916 71

Diabetes is due to an autoimmune cellular immunologic destruction of the pancreatic beta cells. By the use of a chromium release assay and a proliferation assay we have investigated the possible role of beta cell activity for this destruction. Results show that in vitro glucose stimulated pancreatic islet cells are subjects to a slight but significantly higher cellular immunologic destruction by mononuclear spleen cells than unstimulated islet cells. The functional dependency of the islet cell destruction must be a product of both a mononuclear cell dysfunction and a specific islet cell pattern. This is due to the fact that all combinations of mononuclear cells and islet cells from diabetes prone BB rats and non-diabetes prone WF rats tested against each other, results in functional dependent cytotoxicity, except for the assay in which both effector cells and target cells are of WF rat origin. Additional observations indicate, that the diabetes prone BB rat mononuclear cells need previous in vivo activation as only cells from diabetic individuals, and not normoglycemic ones, display the reaction in question. Functional dependent cytotoxicity is validated in an other IDDM animal model--the NOD mouse. NOD mononuclear cells towards the murine MIN-6 beta cell line results in increased cellular cytotoxicity when the latter is glucose stimulated. Also the proliferative response of BB rat mononuclear cells to whole islets tend to show function dependency.
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PMID:Mononuclear cytotoxicity and proliferation towards glucose stimulated rodent pancreatic islet cells. 918 11

The Diabetes Prevention Program is a new, 150 million dollar, NIH-sponsored study designed to determine whether non-insulin-dependent diabetes mellitus can be prevented or delayed in persons with impaired glucose tolerance. Four thousand subjects will be randomly assigned to one of four study groups and followed for 4.5 years. Study groups include intensive lifestyle intervention with diet and exercise; metformin (Glucophage) or troglitazone (an investigational drug) with standard diet and exercise; and a control group. Insulin resistance is an important pathogenic factor in impaired glucose tolerance. Trivalent chromium, a dietary supplement that potentiates the action of insulin, was not included in the program. Like metformin and troglitazone, trivalent chromium decreases insulin resistance and has an acceptable side-effect profile; furthermore, it is available at a fraction of their cost. Trivalent chromium should have been included in the Diabetes Prevention Program; it is unfortunate that it was omitted.
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PMID:Trivalent chromium and the diabetes prevention program. 924 7

Chromium supplementation may affect various risk factors for coronary artery disease (CAD) and non-insulin-dependent diabetes mellitus (NIDDM), including body weight and composition, basal plasma hormone and substrate levels, and response to an oral glucose load. This study examined the effects of chromium supplementation (400 micrograms.d-1), with or without exercise training, on these risk factors in young, obese women. Chromium picolinate supplementation resulted in significant weight gain in this population, while exercise training combined with chromium nicotinate supplementation resulted in significant weight loss and lowered the insulin response to an oral glucose load. We conclude that high levels of chromium picolinate supplementation are contraindicated for weight loss in young, obese women. Moreover, our results suggest that exercise training combined with chromium nicotinate supplementation may be more beneficial than exercise training alone for modification of certain CAD and NIDDM risk factors.
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PMID:Chromium and exercise training: effect on obese women. 926 55

Impaired glycemic control in type II diabetes results from peripheral insulin resistance, hepatic insulin resistance, and a relative failure of beta cell function. Nutritional and pharmaceutical measures are now available for addressing each of these defects, presumably enabling a rational and highly effective clinical management of non-insulin-dependent diabetes mellitus. Peripheral insulin resistance, which usually responds to a very-low-fat diet, aerobic exercise training, and appropriate weight loss, can also treated with high-dose chromium picolinate, high-dose vitamin E, magnesium, soluble fiber, and possibly taurine; these measures appear likely to correct the diabetes-associated metabolic derangements of vascular smooth muscle, and thus lessen risk for macrovascular disease. Metformin's clinical efficacy is primarily reflective of reduced hepatic glucose output; this action should complement the benefits of peripheral insulin sensitizers. When these measures are not sufficient for optimal control, beta cell function can be boosted with second-generation sulfonylureas.
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PMID:Exploiting complementary therapeutic strategies for the treatment of type II diabetes and prevention of its complications. 927 26

Among changes associated with aging is a decline in glucose tolerance. The reported causes are increased insulin resistance from receptor and/or post receptor disturbances and diminished pancreatic islet B-cell sensitivity to glucose. Many recent reports indicate that insulin resistance with hyperinsulinemia and/or hyperglycemia contribute to or even causes many chronic disorders associated with aging, i.e., chronic metabolic perturbations including noninsulin-dependent diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerosis. How could such disturbances in glucose/insulin metabolism lead to many chronic disorders associated with aging? In aging, similar to diabetes, the elevation in circulating glucose and other reducing sugars secondary to age-induced insulin resistance can react nonenzymatically with proteins and nucleic acids to form products that affect function and diminish tissue elasticity. Also, perturbations in glucose/insulin metabolism are associated with enhanced lipid peroxidation secondary to greater free radical formation. Free radicals of oxygen are important known causes of tissue damage and have been associated with many aspects of aging including inflammatory diseases, cataracts, diabetes, and cardiovascular diseases. Augmented free radical formation and lipid peroxidation are not uncommon in diabetes mellitus, commonly associated with "premature aging". Ingestion of sugars, fats, and sodium have been linked to decreased insulin sensitivity, while caloric restriction, exercise, ingestion of chromium, vanadium, soluble fibers, magnesium, and certain antioxidants are associated with greater insulin sensitivity. Thus, manipulation of diet by influencing the glucose/insulin system may favorably affect lifespan and reduce the incidence of chronic disorders associated with aging.
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PMID:Effects of glucose/insulin perturbations on aging and chronic disorders of aging: the evidence. 932 86

Chromium (Cr) improves the glucose/insulin system in subjects with hypoglycemia, hyperglycemia, diabetes and hyperlipemia with no detectable effects on control subjects. Chromium improves insulin binding, insulin receptor number, insulin internalization, beta cell sensitivity and insulin receptor enzymes with overall increases in insulin sensitivity. There have been several studies involving Cr supplementation of subjects with NIDDM and/or lipemia and most have reported beneficial effects of Cr on the glucose/insulin system. In a recent study, Chinese subjects with NIDDM were divided into three groups of 60 subjects and supplemented with placebo, 100 or 500 micrograms of Cr as chromium picolinate 2 times per day for 4 months. Improvements in the glucose/insulin system were highly significant in the subjects receiving 500 micrograms twice per day with less or no significant improvements in the subjects receiving 100 micrograms twice per day after 2 and 4 months. In summary, Cr is involved in the control of the glucose/insulin system and the amount, and likely form of chromium, are critical when evaluating the role of chromium in this system.
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PMID:Nutritional factors influencing the glucose/insulin system: chromium. 932 87

Chromium is an essential nutrient involved in normal carbohydrate and lipid metabolism. The chromium requirement is postulated to increase with increased glucose intolerance and diabetes. The objective of this study was to test the hypothesis that the elevated intake of supplemental chromium is involved in the control of type 2 diabetes. Individuals being treated for type 2 diabetes (180 men and women) were divided randomly into three groups and supplemented with: 1) placebo, 2) 1.92 micromol (100 microg) Cr as chromium picolinate two times per day, or 3) 9.6 micromol (500 microg) Cr two times per day. Subjects continued to take their normal medications and were instructed not to change their normal eating and living habits. HbA1c values improved significantly after 2 months in the group receiving 19.2 pmol (1,000 microg) Cr per day and was lower in both chromium groups after 4 months (placebo, 8.5 +/- 0.2%; 3.85 micromol Cr, 7.5 +/- 0.2%; 19.2 micromol Cr, 6.6 +/- 0.1%). Fasting glucose was lower in the 19.2-micromol group after 2 and 4 months (4-month values: placebo, 8.8 +/- 0.3 mmol/l; 19.2 micromol Cr, 7.1 +/- 0.2 mmol/l). Two-hour glucose values were also significantly lower for the subjects consuming 19.2 micromol supplemental Cr after both 2 and 4 months (4-month values: placebo, 12.3 +/- 0.4 mmo/l; 19.2 micromol Cr, 10.5 +/- 0.2 mmol/l). Fasting and 2-h insulin values decreased significantly in both groups receiving supplemental chromium after 2 and 4 months. Plasma total cholesterol also decreased after 4 months in the subjects receiving 19.2 micromol/day Cr. These data demonstrate that supplemental chromium had significant beneficial effects on HbA1c, glucose, insulin, and cholesterol variables in subjects with type 2 diabetes. The beneficial effects of chromium in individuals with diabetes were observed at levels higher than the upper limit of the Estimated Safe and Adequate Daily Dietary Intake.
Diabetes 1997 Nov
PMID:Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. 935 27


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