A Pilot Study Suggests that the G/G Genotype of Resistin Single Nucleotide Polymorphism at -420 May Be an Independent Predictor of a Reduction in Fasting Plasma Glucose and Insulin Resistance by Pioglitazone in Type 2 Diabetes

Makino, Hideichi; Shimizu, Ikki; Murao, Satoshi; Kondo, Shin‐ichiro; Tabara, Yasuharu; Fujiyama, Masao; Fujii, Yasuhisa; Takada, Yasuharu; Nakai, Kazuaki; Izumi, Kenichi; Ohashi, Jun; Kawamura, Ryuichi; Yamauchi, Junko; Takata, Yasunori; Nishida, Wataru; Hashiramoto, Mitsuru; Onuma, Hiroshi; Osawa, Haruhiko

doi:10.1507/endocrj.k08e-320

Cited by 24 publications

(18 citation statements)

References 41 publications

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“…Moreover, the genetic background of patients could influence in this previous reports as an uncontrolled bias. For example Makino et al [31] demonstrated in patients with diabetes mellitus type 2 that the G/G but not C/G genotype of rs1862513 SNP was correlated with a reduction in fasting plasma glucose and HOMA-IR compared to C/C. When adjusted for age, gender, and BMI, the G/G genotype was an independent factor for the reduction of fasting plasma glucose and HOMA-IR.…”

Section: Discussionmentioning

confidence: 99%

The rs1862513 Variant in Resistin Gene-Modified Insulin Resistance and Insulin Levels after Weight Loss Secondary to Hypocaloric Diet

Luis¹,

Izaola²,

Primo³

et al. 2016

Ann Nutr Metab

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Background/Aims: Polymorphisms of a single nucleotide in RETN have been associated with indexes of insulin resistance. Our aim was to analyze the effects of the rs1862513 RETN gene polymorphism on insulin resistance, insulin levels, and resistin levels changes after 3 months of a low-fat hypocaloric diet. Design: A Caucasian population of 133 obese patients was analyzed before and after 3 months on a low-fat hypocaloric diet. Results: Fifty-six patients (42.1%) had the genotype GG (wild group) and 77 (57.9%) patients had the other genotypes; GC (59 patients, 44.4%) or CC (18 patients, 13.5%; mutant group). In wild and mutant genotype groups, weight, body mass index, fat mass, waist circumference, and systolic blood pressure decreased. In the wild genotype group, the decrease in total cholesterol was -13.1 ± 25.3 mg/dL (vs. -4.4 ± 13.7 mg/dL in mutant group: p = 0.004 for group deltas), low density lipoprotein (LDL)-cholesterol was -13.0 ± 21.5 mg/dL (-4.3 ± 10.5 mg/dL: p = 0.007), glucose -7.2 ± 3.5 mg/dL (-0.8 ± 0.2 mg/dL: p = 0.01), insulin -5.6 ± 2.5 mUI/L (-2.9 ± 1.2 mUI/L: p = 0.03) and homeostasis model assessment-insulin resistance (HOMA-IR) -2.5 ± 1.1 (-0.6 ± 1.4: p = 0.02). Leptin levels decreased in both genotypes (-10.1 ± 9.5 ng/dL in wild type group vs. -13.1 ± 0.2 ng/dL in mutant type group: p > 0.05). Conclusion: The present study suggests that the G/G genotype of RETN rs1862513 could be a predictor of the reduction of HOMA-IR, insulin, fasting glucose and LDL cholesterol secondary to a hypocaloric diet in obese subjects.

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Section: Discussionmentioning

confidence: 99%

The rs1862513 Variant in Resistin Gene-Modified Insulin Resistance and Insulin Levels after Weight Loss Secondary to Hypocaloric Diet

Luis¹,

Izaola²,

Primo³

et al. 2016

Ann Nutr Metab

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“…Additional studies have shown varying levels of evidence for an association between response to TZDs and leptin (115), TNF-a (115) and resistin (116). Although these results are relatively underpowered, they point to the adipokine signaling system and a potential neuroregulatory mechanism underlying TZD response.…”

Section: Adipokinesmentioning

confidence: 99%

The Role of Pharmacogenetics in the Treatment of Diabetes Mellitus / ULOGA FARMAKOGENETIKE U LEČNJU DIJABETES MELITUSA

Topić¹

2014

Journal of Medical Biochemistry

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Summary: Diabetes mellitus is a heterogeneous group of disorders in which particular disease phenotypes can be characterized by a specific etiology and/or pathogenesis of the disease, but in many cases its classification is greatly impeded due to significant phenotype overlapping. Diabetes is a wordwide epidemic with significant health and economic consequences. The frequency of type 2 diabetes (T2D) is much higher than type 1 diabetes (T1D). In adults, around 285 million people suffer from T2DM with a projected rise to 438 million in the next 20 years. A variety of pharmacological treatments exist for patients with T2D, in addition to dietary and physical activity. Pharmacologically, diabetes is treated with nine major classes of approved drugs, including insulin and its analogues, sulfonylureas, biguanides, thiazolidinediones (TZDs), meglitinides, a-glucosidase inhibitors, amylin analogues, incretin hormone mimetics, and dipeptidyl peptidase 4 (DPP4) inhibitors. Treatment strategy for T2D is based mostly on oral hypoglycemic drug (OHD) efficacy assessed usually by HbA1c and/or fasting plasma glucose. The patients are often treated with more than one OHD in combination with the purpose to receive more effective treatment. Characterization of drug response is expected to substantially increase the ability to provide patients with the most effective treatment strategy. If pharmacogenetic testing for diabetes drugs could be used to predict treatment outcome, appropriate measures could be taken to treat T2D more efficiently. To date, major pharmacogenetic studies have focused on response to sulfonylureas, biguanides, and TZDs, the most used OHD. A comprehensive review of the pharmacogenetic studies of specific OHD is presented in this article. Understanding the pharmacogenetics of these drugs Kratak sadr`aj: Dijabetes melitus predstavlja heterogenu grupu pore me}aja u kojoj odre|eni fenotip mo`e karakterisati spe cifi~na etiologija i/ili patogeneza bolesti, ali u mnogim slu~ajevima njegova klasifikacija je vrlo ote`ana zbog zna~ajnog fenotipskog pre klapanja. Dijabetes je globalni epidemiolo{ki problem sa zna~ajnim zdravstvenim i ekonomskim posledicama. U~es talost tipa 2 dijabetesa (T2D) mno go je ve}a od tipa 1 dijabetesa. Kod odraslih, oko 285 miliona osoba boluje od T2D, s predvi|enim rastom do 438 miliona u slede}ih 20 godina. Za pacijente s dijabetesom tipa 2, uz ishranu i fizi~ku aktivnost, postoji niz farmakolo{kih lekova. Devet glavnih vrsta lekova odobreno je za le~enje T2D bolesnika: insulin i njegovi analozi, sulfonilureje, bi gvanidi, tiazolidindioni, meglitinidi, inhibitori a-glukozidaze, analozi amilina, mimetici inkretin hormona i inhibitori dipeptidil-peptidaze 4. Stra te gija le~enja T2D se temelji uglavnom na u~inkovitosti oralnih hipoglikemijskih lekova merenjem HbA1c i/ili glukoze nata{te. Bolesnici se ~esto le~e kombinacijom vi{e oralnih hipoglikemika kako bi se postigla {to uspe{ nija terapija. Ka ra kterizacija odgovora na lek obezbedi}e, kako se o~ekuje, mogu}nost uspe{nijeg leenja, odnosno...

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“…A prospective study of 121 T2DM patients and retrospective data from 63 T2DM patients treated with pioglitazone for 12 weeks revealed that the G/G but not C/G genotype of the resistin gene promoter SNP at −420, rs1862513 had lower FPG ( P =0.020) and better HOMA-IR ( P =0.012) when compared to C/C genotype 31. Patients on rosiglitazone monotherapy (4 mg daily for 12 weeks) with SNP rs11377CC homozygote genotype and 45TG + GG heterozygote genotype of the adiponectin common polymorphisms 45T/G and −11377C/G had a better response in FPG, PPPG, HOMA-IR, and serum adiponectin levels ( P =0.000) compared with 11377CG + GG heterozygote and 45TT homozygote genotypes 32.…”

Section: Thiazolidinedionesmentioning

confidence: 99%

Patient profiling in diabetes and role of canagliflozin

Amblee

2014

PGPM

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Genome-wide association studies have opened the door for patient profiling and research into genetic variants in multifactorial T2DM. Clinically, it may be possible to tailor the type of medication used based on the presence or absence of the various genetic variants. However, the polymorphisms studied may only explain some of the variability in response to T2DM drugs and needs further validation to ensure its authenticity. There are still unidentified factors which appear to play a role in the interindividual variability seen in clinical practice. The potential exists for pharmacogenomics to promote efficacious, safe, and cost-effective individualized diabetes management. Pharmacogenomics is still in its early stages, and the idea of defining patients genetically to predict individual responses to drugs and obtain safe and effective T2DM management is promising, in spite of existing barriers. Currently, clinical profiling of patients with T2DM and using an individualized approach with most drugs, including canagliflozin, based on comorbid conditions still remains the most accepted approach for the management of T2DM.

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A Pilot Study Suggests that the G/G Genotype of Resistin Single Nucleotide Polymorphism at -420 May Be an Independent Predictor of a Reduction in Fasting Plasma Glucose and Insulin Resistance by Pioglitazone in Type 2 Diabetes

Cited by 24 publications

References 41 publications

The rs1862513 Variant in Resistin Gene-Modified Insulin Resistance and Insulin Levels after Weight Loss Secondary to Hypocaloric Diet

The rs1862513 Variant in Resistin Gene-Modified Insulin Resistance and Insulin Levels after Weight Loss Secondary to Hypocaloric Diet

The Role of Pharmacogenetics in the Treatment of Diabetes Mellitus / ULOGA FARMAKOGENETIKE U LEČNJU DIJABETES MELITUSA

Patient profiling in diabetes and role of canagliflozin

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