Risk factor assessment for new onset diabetes: literature review

Bakris, George L.; Stockert, Jack; Molitch, Mark E.; Zhou, Qian; Champion, Annette; Bacher, Peter; Sowers, James R.

doi:10.1111/j.1463-1326.2008.00925.x

Cited by 33 publications

(22 citation statements)

References 67 publications

(97 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Based on data from observational and randomized clinical trials, clinical characteristics known to increase risk for drug induced diabetes include age, ethnicity, race, body mass index, hypertension, stroke, among many others. 9 …”

mentioning

confidence: 99%

Is a Diabetes Mellitus–Linked Amino Acid Signature Associated With β-Blocker–Induced Impaired Fasting Glucose?

Cooper‐DeHoff

Hou

Weng

et al. 2014

Circ Cardiovasc Genet

View full text Add to dashboard Cite

Background The five amino acid (AA) signature including isoleucine (Ile), leucine (Leu), valine (Val), tyrosine (Tyr), and phenylalanine (Phe) has been associated with incident diabetes and insulin resistance. We investigated whether this same AA signature, single nucleotide polymorphisms (SNPs) in genes in their catabolic pathway, were associated with development of impaired fasting glucose (IFG) after atenolol treatment. Methods and Results Among 234 European American participants enrolled in the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) study and treated with atenolol for 9 weeks, we prospectively followed a nested cohort that had both metabolomics profiling and genotype data available, for the development of IFG. We assessed the association between baseline circulating levels of Ile, Leu, Val, Tyr and Phe, as well as SNPs in BCAT1 and PAH with development of IFG. All baseline AA levels were strongly associated with IFG development. Each increment in standard deviation of the five AAs was associated with the following odds ratio and 95% confidence interval for IFG based on fully adjusted model: Ile 2.29 (1.31–4.01), Leu 1.80 (1.10–2.96), Val 1.77 (1.07–2.92), Tyr 2.13 (1.20–3.78) and Phe 2.04 (1.16–3.59). The composite p value was 2x10−5. Those with PAH (rs2245360) AA genotype had the highest incidence of IFG (p for trend=0.0003). Conclusions Our data provide important insight into the metabolic and genetic mechanisms underlying atenolol associated adverse metabolic effects. Clinical Trial Registration clinicaltrials.gov; Unique Identifier: NCT00246519

show abstract

mentioning

confidence: 99%

Is a Diabetes Mellitus–Linked Amino Acid Signature Associated With β-Blocker–Induced Impaired Fasting Glucose?

Cooper‐DeHoff

Hou

Weng

et al. 2014

Circ Cardiovasc Genet

View full text Add to dashboard Cite

show abstract

“…But individuals who are not considered obese may also exhibit physiological alterations similar to those seen in obesity including insulin resistance (resulting in impaired glucose tolerance), visceral adiposity and dyslipidemia (elevated levels triglycerides and LDL cholesterol, and decreased levels of HDL). The later phenotype, which has been dubbed the “metabolic syndrome” (MS), predisposes to several major age-related diseases including diabetes (Bakris et al, 2008), cardiovascular disease (Aggoun, 2007), stroke (Gil-Nunez, 2007) and possibly cognitive impairment and Alzheimer’s disease (Pasinetti and Eberstein, 2008; Stranahan et al, 2008). The prevalence of MS and obesity have increased rapidly in the past 30 years, tripling in adolescents between 1970 and 2000 (Harrell et al, 2006), heightening the importance of understanding the cellular and molecular mechanisms by which these conditions promote disease.…”

Section: The Metabolic Syndromementioning

confidence: 99%

Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders

Mattson

2009

Experimental Gerontology

262

205

View full text Add to dashboard Cite

A rising tide of obesity and type 2 diabetes has resulted from the development of technologies that have made inexpensive high calorie foods readily available and exercise unnecessary for many people. Obesity and the metabolic syndrome (insulin resistance, visceral adiposity and dyslipidemia) wreak havoc on cells throughout the body thereby promoting cardiovascular and kidney disease, and degenerative diseases of the brain and body. Obesity and insulin resistance promote disease by increasing oxidative damage to proteins, lipids and DNA as the result of a combination of increased free radical production and an impaired ability of cells to detoxify the radicals and repair damaged molecules. By covalently modifying membrane-associated proteins, the membrane lipid peroxidation product 4-hydroxynonenal (HNE) may play particularly sinister roles in the metabolic syndrome and associated disease processes. HNE can damage pancreatic β cells and can impair the ability of muscle and liver cells to respond to insulin. HNE may promote atherosclerosis by modifying lipoproteins and can cause cardiac cell damage by impairing metabolic enzymes. An adverse role for HNE in the brain in obesity and the metabolic syndrome is suggested by studies showing that HNE levels are increased in brain cells with aging and Alzheimer's disease. HNE can cause the dysfunction and degeneration of neurons by modifying membrane-associated glucose and glutamate transporters, ion-motive ATPases, enzymes involved in amyloid metabolism, and cytoskeletal proteins. Exercise and dietary energy restriction reduce HNE production and may also increase cellular systems for HNE detoxification including glutathione and oxidoreductases. The recent development of low molecular weight molecules that scavenge HNE suggests that HNE can be targeted in the design of drugs for the treatment of obesity, the metabolic syndrome, and associated disorders.

show abstract

“…Nevertheless, impairment of glucose metabolism during the OGTT, especially when combined with the fasting and first-phase insulin responses, are a good, arguably the best, predictor for type 2 diabetes mellitus. 10,38,39 We used OGTT as our primary outcome measure because, in a multiple crossover study, a relatively simple and well-tolerated procedure is required to retain subject participation. Glucose-clamp techniques may be useful in further studies to investigate the pathophysiological mechanisms.…”

Section: Potential Limitations Of Studymentioning

confidence: 99%

A Double-Blind, Placebo-Controlled, Crossover Trial Comparing the Effects of Amiloride and Hydrochlorothiazide on Glucose Tolerance in Patients With Essential Hypertension

et al. 2012

View full text Add to dashboard Cite

Abstract-Hypertension guidelines advise limiting the dose of thiazide diuretics and avoiding combination with ␤-blockade, because of increased risk of diabetes mellitus. We tested whether changes in the 2-hour oral glucose tolerance test could be detected after 4 weeks of treatment with a thiazide and could be avoided by switching to amiloride. Two double-blind, placebo-controlled, crossover studies were performed. In study 1 (41 patients), we found that changes in glucose during a 2-hour oral glucose tolerance test could be detected after 4 weeks of treatment with bendroflumethiazide. In study 2, 37 patients with essential hypertension received, in random order, 4 weeks of once-daily treatment with hydrochlorothiazide (HCTZ) 25 to 50 mg, nebivolol 5 to 10 mg, combination (HCTZ 25-50 mgϩnebivolol 5-10 mg), amiloride (10 -20 mg), and placebo. Each drug was force titrated at 2 weeks and separated by a 4-week placebo washout. At each visit, we recorded blood pressure and performed a 75-g oral glucose tolerance test. Primary outcome was the difference in glucose (over the 2 hours of the oral glucose tolerance test) between 0 and 4 weeks, when HCTZ and amiloride were compared by repeated-measures analysis. For similar blood pressure reductions, there were opposite changes in glucose between the 2 diuretics (PϽ0.0001). Nebivolol did not impair glucose tolerance, either alone or in combination. There was a negative correlation between ⌬potassium and ⌬2-hour glucose (rϭϪ0.28; PϽ0.0001). In 2 crossover studies, 4 weeks of treatment with a thiazide diuretic impaired glucose tolerance. No impairment was seen with K 1 Outcome trials have shown cardiovascular benefits from the use of thiazides in essential hypertension, which are similar to those achieved with other antihypertensive agents. However, there has been recent recognition that currently used doses are smaller than those used in most of the outcome trials.3-5 The main adverse effects limiting the use of thiazides are metabolic, including hypokalemia, hyponatremia, hyperuricemia, and hyperglycemia.

show abstract

Risk factor assessment for new onset diabetes: literature review

Cited by 33 publications

References 67 publications

Is a Diabetes Mellitus–Linked Amino Acid Signature Associated With β-Blocker–Induced Impaired Fasting Glucose?

Is a Diabetes Mellitus–Linked Amino Acid Signature Associated With β-Blocker–Induced Impaired Fasting Glucose?

Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders

A Double-Blind, Placebo-Controlled, Crossover Trial Comparing the Effects of Amiloride and Hydrochlorothiazide on Glucose Tolerance in Patients With Essential Hypertension

Contact Info

Product

Resources

About