Evidence map›Paper›PMID 24957168›Full record

ArticleJournal of endocrinological investigation2014

The effect of leptin promoter and leptin receptor gene polymorphisms on lipid profile among the diabetic population: modulations by atorvastatin treatment and environmental factors.

Sayer I Al-Azzam, Omar F Khabour, Karem H Alzoubi, Raya N Alzayadeen

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Article in Journal of endocrinological investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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3citing papers in PubMed
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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Epigenetics: spotlight on type 2 diabetes and obesity.Journal of endocrinological investigation · 2016
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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Sayer I Al-AzzamDepartment of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, 22110, Jordan.
Omar F Khabour
Karem H Alzoubi
Raya N Alzayadeen

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThis study investigated the effect of leptin (LEP) 2548A/G and leptin receptor (LEPR) Q223R polymorphisms on the levels of HDL, LDL, TG, and total cholesterol (t-chol). In addition, the interactions between examined polymorphisms, statin therapy and environmental factors on lipid profile were examined.

methodsAdult diabetic patients (n-418) were recruited from diabetes/endocrine clinics in north of Jordan. Lipid profile was measured using standard protocols. Genotyping of LEP 2548A/G and LEPR Q223R polymorphisms was carried out using polymerase chain reaction-restriction fragment length polymorphisms.

resultsNo significant association between LEP 2548A/G and LEPR genotypes and levels of HDL (P = 0.83), LDL (P = 0.40), TG (P = 0.23) and t-chol (P = 0.91). However, in patient on atorvastatin, those with GG or GA genotypes of LEP 2548 experienced significantly higher levels of LDL compared with AA genotype of LEP 2548 (P < 0.002). Patients with dyslipidemia had higher TG in comparison with those without (P < 0.03). Smokers had lower HDL and higher TG levels compared with none smokers or previous smokers (P < 0.002 and P < 0.02, respectively). Female patients tend to have a higher HDL in comparison with male patients (P < 0.05). Patients with HbA1c value greater than or equal to 7 had higher LDL and t-chol compared with patients who had an HbA1c levels of <7 (P < 0.02 and < 0.005, respectively). Patients with disease duration of 5 or more years had a lower HDL compared with those patients with duration of <5 years (P < 0.03).

conclusionIn conclusion, and although lipid profile regulation is a multifactorial process, -2548G/A LEP polymorphism seems to affect statins treatment response among diabetic patients. More studies are required to specifically define factors that influence lipid profiles interaction with statin treatment response especially among patients with diabetes.

Indexed as

Diabetes Mellitus, Type 2DyslipidemiasAtorvastatinCholesterolCholesterol, HDLCholesterol, LDLFemaleGene-Environment InteractionGenotypeGlycated HemoglobinHeptanoic AcidsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLeptinMaleMiddle AgedAtorvastatinCholesterolCholesterol, HDLCholesterol, LDLGlycated Hemoglobinhemoglobin A1c protein, humanHeptanoic AcidsHydroxymethylglutaryl-CoA Reductase InhibitorsLEPR protein, humanLeptinPyrrolesReceptors, LeptinTriglycerides

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.