The influence of the Pro12Ala mutation of the PPAR‐gamma receptor gene on metabolic and clinical characteristics in treatment‐naïve patients with type 2 diabetes

Ahluwalia, Maninder; Evans, Marc; Morris, Keith; Currie, Craig John; Davies, Sara; Rees, A.; Thomas, Andrew W.

doi:10.1046/j.1463-1326.2002.00230.x

Cited by 18 publications

(10 citation statements)

References 9 publications

(8 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Potentially, a mechanism including higher leptin levels and leptin resistance may explain higher fat intakes in obese individuals carrying the Ala12 allele. PPAR γ Pro12Ala has been inconsistently associated with BMI [58,67,68]. In the present study, BMI and energy intakes were comparable between genotypes.…”

Section: Discussionsupporting

confidence: 52%

Associations between Polymorphisms in Genes Involved in Fatty Acid Metabolism and Dietary Fat Intakes

Bouchard-Mercier¹,

Paradis²,

Pérusse³

et al. 2012

Lifestyle Genomics

View full text Add to dashboard Cite

Background: Obesity prevalence is growing in our population. Twin studies have estimated the heritability of dietary intakes to about 30%. The objective of this study was to verify whether polymorphisms in genes involved in fatty acid metabolism are associated with dietary fat intakes. Methods: Seven hundred participants were recruited. A validated food frequency questionnaire was used to assess dietary intakes. PCR-RFLP and TAQMAN methodology were used to genotype PPARα Leu162Val, PPARγ Pro12Ala, PPARδ –87T>C, PPARGC1α Gly482Ser, FASN Val1483Ile and SREBF1 c.*619C>G. Statistical analyses were executed with SAS statistical package. Results: Carriers of the Ala12 allele of PPARγ Pro12Ala polymorphism had higher intakes of total fat (p = 0.04). For FASN Val1483Ile polymorphism, significant gene-sex interaction effects were found for total fat and saturated fat intakes (p = 0.02 and p = 0.002, respectively). No significant difference in fat intakes was observed for PPARα Leu162Val, PPARδ –87T>C, PPARGC1α Gly482Ser and SREBF1 c.*619C>G polymorphisms. Conclusions: Polymorphisms in PPARγ and FASN seem to be associated with dietary fat intakes. Genetic variants are important to take into account when studying dietary intakes.

show abstract

Section: Discussionsupporting

confidence: 52%

Associations between Polymorphisms in Genes Involved in Fatty Acid Metabolism and Dietary Fat Intakes

Bouchard-Mercier¹,

Paradis²,

Pérusse³

et al. 2012

Lifestyle Genomics

View full text Add to dashboard Cite

show abstract

“…Many molecules are involved in the differentiation of preadipocytes into mature adipocytes. C/EBPα and PPARγ play important roles among these molecules: PPARγ can induce the maturation of adipocytes and regulate the expression of adipogenesis-related genes, whereas C/EBPα can regulate the terminal differentiation of adipocytes (12)(13)(14)(15). Thus, the overdifferentiation of adipocytes and abnormal deposition of adipose tissues might be related to the increased expression of C/EBPα and PPARγ.…”

Section: Discussionmentioning

confidence: 99%

Effects of SOCS 1/3 gene silencing on the expression of C/EBPα and PPARγ during differentiation and maturation of rat preadipocytes

Zheng

Liao

et al. 2012

Pediatr Res

View full text Add to dashboard Cite

Background: suppressor of cytokine signaling-1 and -3 (sOcs-1 and sOcs-3) are two important negative regulators in the insulin-signaling pathway, and their overexpression may aggravate insulin resistance. subjects with insulin resistance are often obese and have increased expressions of sOcs-1 and sOcs-3. We speculated that sOcs-1 and sOcs-3 may be involved in abnormal deposition of adipose tissues during insulin resistance. Methods: a catch-up growth intrauterine growth retardation (cG-IUGR) rat model with insulin resistance was established; mRNa and protein expression of sOcs-1, sOcs-3, the ccaaT/enhancer binding protein (c/eBPα), and peroxisome proliferator-activated receptor (PPaRγ) in adipose tissue were measured by real-time PcR and western blot; plasmids carrying small hairpin RNas (shRNas) targeting the SOCS-1and SOCS-3 genes were constructed and transfected into preadipocytes, which were then induced to mature. at 72 h after differentiation was induced, the expressions of c/eBPα and PPaRγ, two important molecules promoting the differentiation of preadipocytes, were detected. results: expressions of sOcs-1, sOcs-3, c/eBPα, and PPaRγ were markedly increased in adipose tissues of cG-IUGR rats, whereas the expressions of c/eBPα and PPaRγ were significantly reduced after gene silencing of SOCS-1 or SOCS-3 in adipocytes. conclusion: Overexpression of sOcs-1 and sOcs-3 may enhance the expression of c/eBPα and PPaRγ, resulting in abnormal deposition of adipose tissues during insulin resistance.

show abstract

“…In addition to the positive studies summarized above, we identified 40 studies dealing with 27 candidate genes in which there were no associations between DNA sequence variations and obesity‐related phenotypes. Among these studies, the most frequent were those pertaining to markers of UCP2 (142, 143, 144, 145) (four studies), ADRA2B (146, 147, 148), ADRB2 (149, 150, 151), PPARG (86, 152, 153), and RETN (154, 155, 156) (three studies each). Other markers yielding negative findings were those related to ACE (157), ADRB3 (158), APOE (159, 160), CAPN10 (161), CYP27B1 (162), DGAT1 (163), DRD2 (164), EDN1 (165, 166), ESR1 (167), F7 (168), FABP2 (169), GNB3 (170), GPR10 (171), IL6 (172, 173), IRS1 (174), IRS2 (174), LEPR (175), LPL (176), NOS3 (177), NR0B2 (178), SORBS1 (179), and TNF (180).…”

Section: Qtls From Crossbreeding Experimentsmentioning

confidence: 99%

The Human Obesity Gene Map: The 2003 Update

et al. 2004

View full text Add to dashboard Cite

This is the tenth update of the human obesity gene map, incorporating published results up to the end of October 2003 and continuing the previous format. Evidence from single‐gene mutation obesity cases, Mendelian disorders exhibiting obesity as a clinical feature, quantitative trait loci (QTLs) from human genome‐wide scans and animal crossbreeding experiments, and association and linkage studies with candidate genes and other markers is reviewed. Transgenic and knockout murine models relevant to obesity are also incorporated (N = 55). As of October 2003, 41 Mendelian syndromes relevant to human obesity have been mapped to a genomic region, and causal genes or strong candidates have been identified for most of these syndromes. QTLs reported from animal models currently number 183. There are 208 human QTLs for obesity phenotypes from genome‐wide scans and candidate regions in targeted studies. A total of 35 genomic regions harbor QTLs replicated among two to five studies. Attempts to relate DNA sequence variation in specific genes to obesity phenotypes continue to grow, with 272 studies reporting positive associations with 90 candidate genes. Fifteen such candidate genes are supported by at least five positive studies. The obesity gene map shows putative loci on all chromosomes except Y. Overall, more than 430 genes, markers, and chromosomal regions have been associated or linked with human obesity phenotypes. The electronic version of the map with links to useful sites can be found at http://obesitygene.pbrc.edu.

show abstract

The influence of the Pro12Ala mutation of the PPAR‐gamma receptor gene on metabolic and clinical characteristics in treatment‐naïve patients with type 2 diabetes

Cited by 18 publications

References 9 publications

Associations between Polymorphisms in Genes Involved in Fatty Acid Metabolism and Dietary Fat Intakes

Associations between Polymorphisms in Genes Involved in Fatty Acid Metabolism and Dietary Fat Intakes

Effects of SOCS 1/3 gene silencing on the expression of C/EBPα and PPARγ during differentiation and maturation of rat preadipocytes

The Human Obesity Gene Map: The 2003 Update

Contact Info

Product

Resources

About