Glucose metabolism disorders -
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Full Format Full Full text Summary Summary text. Choose Destination File Clipboard Collections Format Full text Summary text Create File. Chemicals in your digestive system enzymes break the food parts down into sugars and acids, your body's fuel.
Your body can use this fuel right away, or it can store the energy in your body tissues. If you have a metabolic disorder , something goes wrong with this process.
Carbohydrate metabolism disorders are a group of metabolic disorders. Normally your enzymes break carbohydrates down into glucose a type of sugar.
If you have one of these disorders, you may not have enough enzymes to break down the carbohydrates. Or the enzymes may not work properly. This causes a harmful amount of sugar to build up in your body.
That can lead to health problems, some of which can be serious. Some of the disorders are fatal. These disorders are inherited. Newborn babies get screened for many of them, using blood tests. If there is a family history of one of these disorders, parents can get genetic testing to see whether they carry the gene.
Other genetic tests can tell whether the fetus has the disorder or carries the gene for the disorder. Evaluation of Patients. Note added in proof. Journal Article. Disorders of Glucose Metabolism in Patients Infected with Human Immunodeficiency Virus.
Dubé Michael P. Department of Medicine and Division of Infectious Diseases, Indiana University School of Medicine. Oxford Academic.
Revision received:. PDF Split View Views. Cite Cite Michael P. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote. bibtex BibTex. txt Medlars, RefWorks Download citation.
Permissions Icon Permissions. Close Navbar Search Filter Clinical Infectious Diseases This issue IDSA Journals Infectious Diseases Books Journals Oxford Academic Enter search term Search. Figure 1. Open in new tab Download slide. Table 1 Evidence for and against the notion that human immunodeficiency virus HIV protease inhibitors PIs are primarily responsible for glucose metabolism abnormalities in antiretroviral-treated HIV-infected patients.
Open in new tab. Figure 2. Table 2 Drugs other than protease inhibitors that are commonly used in the treatment of patients infected with human immunodeficiency virus and may alter glucose metabolism.
Agent Mechanism Glucocorticoid Insulin resistance Megesterol acetate Insulin resistance Human growth hormone Insulin resistance Androgenic steroid a Insulin resistance Pentamidine B-cell dysfunction Didanosine B-cell dysfunction.
a May increase or ameliorate insulin resistance, depending on the setting. Table 3 Major risk factors for type 2 diabetes mellitus. Reports of diabetes and hyperglycemia in patients receiving protease inhibitors for the treatment of human immunodeficiency virus HIV.
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Treatment with protease inhibitors associated with peripheral insulin resistance and impaired oral glucose tolerance in HIVinfected patients. Hyperlipidemia and insulin resistance are induced by protease inhibitors independent of changes in body composition in patients with HIV infection.
A syndrome of peripheral lipodystrophy, hyperlipidaemia, and insulin resistance due to HIV protease inhibitors. Impaired glucose tolerance, beta cell function and lipid metabolism in HIV patients under treatment with protease inhibitors.
Effect of initiating indinavir therapy on glucose metabolism in HIV-infected patients: results of minimal model analysis. Google Scholar OpenURL Placeholder Text. Fasting hyperinsulinemia and changes in regional body composition in human immunodeficiency virus-infected women.
Google Scholar PubMed. OpenURL Placeholder Text. Fasting hyperinsulinemia in human immunodeficiency virus-infected men: relationship to body composition, gonadal function, and protease inhibitor use. Fasting hyperinsulinemia and increased waist-to-hip ratios in non-wasting individuals with AIDS.
Preliminary guidelines for the evaluation and management of dyslipidemia in HIV-infected adults receiving antiretroviral therapy: recommendations of the Adult ACTG Cardiovascular Disease Focus Group. Insulin resistance implications for type II diabetes mellitus and coronary heart disease.
Diagnosis, prediction, and natural course of HIV-1 protease-inhibitor-associated lipodystrophy, hyperlipidaemia, and diabetes mellitus: a cohort study.
Diabetes and hyperglycemia in patients receiving protease inhibitors [abstract ]. Program and abstracts of the 5th Conference on Retroviruses and Opportunistic Infections Chicago.
Reversion of metabolic abnormalities after switching from HIV-1 protease inhibitors to nevirapine. The short insulin tolerance test for determination of insulin sensitivity: a comparison with the euglycemic clamp.
The pathophysiology of type II noninsulin dependent diabetes mellitus: implications for treatment. Homeostasis model assessment: insulin resistance and B-cell function from fasting plasma glucose and insulin concentrations in man.
Endocrine and metabolic evaluation of human immunodeficiency virus-infected patients with evidence of protease inhibitor-associated lipodystrophy. Lipodystrophy defined by a clinical score in HIV-infected men on highly active antiretroviral therapy: correlation between dyslipidaemia and steroid hormone alterations.
Equivalence of the insulin sensitivity index in man derived by the minimal model method and the euglycemic glucose clamp. The mechanism of insulin resistance caused by HIV protease inhibitor therapy.
A novel use of abacavir to simplify therapy in PI experienced patients successfully treated with HAART [abstract CNA]. Program and abstracts of the 7th Conference on Retroviruses and Opportunistic Infections San Francisco.
Effects of aerosolized pentamidine on glucose homeostasis and insulin secretion in HIV-positive patients: a controlled study. Pentamidine-induced derangements of glucose homeostasis: determinant roles of renal failure and drug accumulation: a study of patients.
Hypoglycemia and diabetes mellitus following parenteral pentamidine mesylate treatment in AIDS patients. Diabetes mellitus in a patient with AIDS after treatment with pentamidine aerosol. Severe hyperglycemia in an HIV clinic: preexisting versus drug-associated diabetes mellitus.
Transient insulin-dependent diabetes mellitus in an HIV-infected patient receiving didanosine. Hyperosmolar nonketotic diabetic syndrome following treatment of human immunodeficiency virus infection with didanosine.
The use and toxicity of didanosine ddI in HIV antibody-positive individuals intolerant to zidovudine AZT. Insulin sensitivity and insulin clearance in human immunodeficiency virus-infected men. Pancreatic beta-cell dysfunction as the primary genetic lesion in NIDDM: evidence from studies in normal glucose-tolerant individuals with a first-degree NIDDM relative.
Earlier appearance of impaired insulin secretion than of visceral adiposity in the pathogenesis of NIDDM: 5-year follow-up of initially nondiabetic Japanese-American men.
Changes in body habitus and serum lipid abnormalities in HIV-positive women on highly active antiretroviral therapy HAART. Diabetes, insulin resistance and dyslipidaemia in lipodystrophic HIV-infected patients on highly active antiretroviral therapy HAART. Redistribution of body fat in HIV-infected women undergoing combined antiretroviral therapy.
A syndrome of peripheral fat wasting lipodystrophy in patients receiving long-term nucleoside analogue therapy. A syndrome of lipoatrophy, lactic acidaemia and liver dysfunction associated with HIV nucleoside analogue therapy: contribution to protease inhibitor-related lipodystrophy syndrome.
Mitochondrial toxicity induced by nucleoside-analogue reverse-transcriptase inhibitors is a key factor in the pathogenesis of antiretroviral-therapy-related lipodystrophy. The effects of discontinuing stavudine therapy on clinical and metabolic abnormalities in patients suffering from lipodystrophy.
A prospective, open-label pilot trial of a maintenance nevirapine-containing regimen in patients with undetectable viral loads on protease inhibitor regimens for at least 6 months [abstract 45].
Impact of switching from HIV-1 protease inhibitors PI to efavirenz EFV in patients with lipodystrophy [abstract 50]. Protease inhibitor-associated hyperglycemia: results of switching from indinavir to nelfinavir [abstract ]. High fat diet and susceptibility to obesity increase the effects of HIV protease inhibitors on metabolism in mice [abstract 37].
Hyperlactatemia in 20 patients receiving NRTI combination regimens [abstract 56]. Effect of troglitazone on body fat distribution in type 2 diabetic patients. Activators of peroxisome proliferator-activated receptor gamma have depot-specific effects on human preadipocyte differentiation.
Hepatotoxicity due to troglitazone: report of two cases and review of adverse events reported to the United States Food and Drug Administration. Hepatocellular injury in a patient receiving rosiglitazone: a case report.
Effects of metformin on insulin resistance and central adiposity in patients receiving effective protease inhibitor therapy.
Physical activity and cardiovascular health. NIH Consensus Development Panel on Physical Activity and Cardiovascular Health. Nutrition recommendations and principles for people with diabetes mellitus.
Resistance exercise training reduces hypertriglyceridemia in HIV-infected men treated with antiviral therapy [abstract 54]. Kenneth H. Mayer, Section Editor. Issue Section:. Download all slides. Comments 0. Add comment Close comment form modal. I agree to the terms and conditions.
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Michael P. However, metwbolism resistance and impaired glucose tolerance will develop during PI treatment fisorders Diet and weight control considerable Idsorders of patients. Dyslipidemia, abdominal obesity, disirders loss of Glucoae Sport-Specific Drills and Techniques frequently coexist with insulin resistance, but it is not clear whether all of these result from a common pathogenic mechanism. Recent data suggest that insulin resistance may also be associated with HIV infection in patients not receiving PI therapy. The long-term consequences of insulin resistance in this population are not known. The effect of switching to other antiretroviral therapies has not been fully determined.
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