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Association of Neuropeptide-Y (NPY) and Interleukin-1beta (IL1B), Genotype-Phenotype Correlation and Plasma Lipids with Type-II Diabetes
Neuropeptide Y (NPY) is known to play a role in the regulation of satiety, energy balance, body weight, and insulin release. Interleukin-1beta (IL1B) has been associated with loss of beta-cell mass in type-II diabetes (TIID). The present study attempts to investigate the association of NPY exon2 +11...
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| Published in: | PloS one 2016-10, Vol.11 (10), p.e0164437-e0164437 |
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| creator | Patel, Roma Dwivedi, Mitesh Mansuri, Mohmmad Shoab Ansarullah Laddha, Naresh C Thakker, Ami Ramachandran, A V Begum, Rasheedunnisa |
| description | Neuropeptide Y (NPY) is known to play a role in the regulation of satiety, energy balance, body weight, and insulin release. Interleukin-1beta (IL1B) has been associated with loss of beta-cell mass in type-II diabetes (TIID).
The present study attempts to investigate the association of NPY exon2 +1128 T/C (Leu7Pro; rs16139), NPY promoter -399 T/C (rs16147) and IL1B -511 C/T (rs16944) polymorphisms with TIID and their correlation with plasma lipid levels, BMI, and IL1B transcript levels.
PCR-RFLP was used for genotyping these polymorphisms in a case-control study involving 558 TIID patients and 1085 healthy age-matched controls from Gujarat. Linkage disequilibrium and haplotype analysis of the NPY polymorphic sites were performed to assess their association with TIID. IL1B transcript levels in PBMCs were also assessed in 108 controls and 101 patients using real-time PCR.
Our results show significant association of both structural and promoter polymorphisms of NPY (p |
| doi_str_mv | 10.1371/journal.pone.0164437 |
| format | article |
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The present study attempts to investigate the association of NPY exon2 +1128 T/C (Leu7Pro; rs16139), NPY promoter -399 T/C (rs16147) and IL1B -511 C/T (rs16944) polymorphisms with TIID and their correlation with plasma lipid levels, BMI, and IL1B transcript levels.
PCR-RFLP was used for genotyping these polymorphisms in a case-control study involving 558 TIID patients and 1085 healthy age-matched controls from Gujarat. Linkage disequilibrium and haplotype analysis of the NPY polymorphic sites were performed to assess their association with TIID. IL1B transcript levels in PBMCs were also assessed in 108 controls and 101 patients using real-time PCR.
Our results show significant association of both structural and promoter polymorphisms of NPY (p<0.0001 and p<0.0001 respectively) in patients with TIID. However, the IL1B C/T polymorphism did not show any association (p = 0.3797) with TIID patients. Haplotype analysis revealed more frequent association of CC and CT haplotypes (p = 3.34 x 10-5, p = 6.04 x 10-9) in diabetics compared to controls and increased the risk of diabetes by 3.02 and 2.088 respectively. Transcript levels of IL1B were significantly higher (p<0.0001) in patients as compared to controls. Genotype-phenotype correlation of IL1B polymorphism did not show any association with its higher transcript levels. In addition, NPY +1128 T/C polymorphism was found to be associated with increased plasma LDL levels (p = 0.01).
The present study provides an evidence for a strong correlation between structural and promoter polymorphisms of NPY gene and upregulation of IL1B transcript levels with susceptibility to TIID and altering the lipid metabolism in Gujarat population.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0164437</identifier><identifier>PMID: 27749914</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Alleles ; Beta cells ; Biochemistry ; Biology and Life Sciences ; Blood Glucose - analysis ; Body mass ; Body Mass Index ; Body weight ; Cardiovascular disease ; Case-Control Studies ; Cholesterol ; Correlation ; Cytokines ; Deoxyribonucleic acid ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - pathology ; Diabetic retinopathy ; DNA ; Energy balance ; Exons ; Female ; Gene Frequency ; Gene polymorphism ; Genetic Association Studies ; Genotype ; Genotyping ; Haplotypes ; Health risks ; Humans ; Insulin ; Insulin resistance ; Interleukin ; Interleukin 1 ; Interleukin-1beta - genetics ; Interleukin-1beta - metabolism ; Linkage analysis ; Linkage Disequilibrium ; Lipid metabolism ; Lipids ; Lipids - blood ; Lipoproteins ; Lipoproteins (low density) ; Lipoproteins, LDL - blood ; Low density lipoprotein ; Male ; Males ; Medicine and Health Sciences ; Metabolism ; Middle Aged ; Neuropeptide Y ; Neuropeptide Y - genetics ; Neuropeptide Y - metabolism ; Neuropeptides ; Nutrition research ; Patients ; Phenotypes ; Polymerase chain reaction ; Polymorphism ; Polymorphism, Single Nucleotide ; Population ; Promoter Regions, Genetic ; Real-Time Polymerase Chain Reaction ; Research and Analysis Methods ; Restriction fragment length polymorphism ; Risk ; Risk management ; RNA, Messenger - metabolism ; Rodents ; Satiety ; Science ; Transcription ; Triglycerides - blood ; Zoology</subject><ispartof>PloS one, 2016-10, Vol.11 (10), p.e0164437-e0164437</ispartof><rights>2016 Patel et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Patel et al 2016 Patel et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-7cdea0f168dda4639da10879e9022451fec66735b08a5251cb3eeb8313c307723</citedby><cites>FETCH-LOGICAL-c559t-7cdea0f168dda4639da10879e9022451fec66735b08a5251cb3eeb8313c307723</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1829760763/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1829760763?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25752,27923,27924,37011,37012,44589,53790,53792,74897</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27749914$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Grolmusz, Vince</contributor><creatorcontrib>Patel, Roma</creatorcontrib><creatorcontrib>Dwivedi, Mitesh</creatorcontrib><creatorcontrib>Mansuri, Mohmmad Shoab</creatorcontrib><creatorcontrib>Ansarullah</creatorcontrib><creatorcontrib>Laddha, Naresh C</creatorcontrib><creatorcontrib>Thakker, Ami</creatorcontrib><creatorcontrib>Ramachandran, A V</creatorcontrib><creatorcontrib>Begum, Rasheedunnisa</creatorcontrib><title>Association of Neuropeptide-Y (NPY) and Interleukin-1beta (IL1B), Genotype-Phenotype Correlation and Plasma Lipids with Type-II Diabetes</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Neuropeptide Y (NPY) is known to play a role in the regulation of satiety, energy balance, body weight, and insulin release. Interleukin-1beta (IL1B) has been associated with loss of beta-cell mass in type-II diabetes (TIID).
The present study attempts to investigate the association of NPY exon2 +1128 T/C (Leu7Pro; rs16139), NPY promoter -399 T/C (rs16147) and IL1B -511 C/T (rs16944) polymorphisms with TIID and their correlation with plasma lipid levels, BMI, and IL1B transcript levels.
PCR-RFLP was used for genotyping these polymorphisms in a case-control study involving 558 TIID patients and 1085 healthy age-matched controls from Gujarat. Linkage disequilibrium and haplotype analysis of the NPY polymorphic sites were performed to assess their association with TIID. IL1B transcript levels in PBMCs were also assessed in 108 controls and 101 patients using real-time PCR.
Our results show significant association of both structural and promoter polymorphisms of NPY (p<0.0001 and p<0.0001 respectively) in patients with TIID. However, the IL1B C/T polymorphism did not show any association (p = 0.3797) with TIID patients. Haplotype analysis revealed more frequent association of CC and CT haplotypes (p = 3.34 x 10-5, p = 6.04 x 10-9) in diabetics compared to controls and increased the risk of diabetes by 3.02 and 2.088 respectively. Transcript levels of IL1B were significantly higher (p<0.0001) in patients as compared to controls. Genotype-phenotype correlation of IL1B polymorphism did not show any association with its higher transcript levels. In addition, NPY +1128 T/C polymorphism was found to be associated with increased plasma LDL levels (p = 0.01).
The present study provides an evidence for a strong correlation between structural and promoter polymorphisms of NPY gene and upregulation of IL1B transcript levels with susceptibility to TIID and altering the lipid metabolism in Gujarat population.</description><subject>Adult</subject><subject>Alleles</subject><subject>Beta cells</subject><subject>Biochemistry</subject><subject>Biology and Life Sciences</subject><subject>Blood Glucose - analysis</subject><subject>Body mass</subject><subject>Body Mass Index</subject><subject>Body weight</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Cholesterol</subject><subject>Correlation</subject><subject>Cytokines</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetic retinopathy</subject><subject>DNA</subject><subject>Energy balance</subject><subject>Exons</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Gene polymorphism</subject><subject>Genetic Association Studies</subject><subject>Genotype</subject><subject>Genotyping</subject><subject>Haplotypes</subject><subject>Health risks</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Interleukin</subject><subject>Interleukin 1</subject><subject>Interleukin-1beta - genetics</subject><subject>Interleukin-1beta - metabolism</subject><subject>Linkage analysis</subject><subject>Linkage Disequilibrium</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Lipids - blood</subject><subject>Lipoproteins</subject><subject>Lipoproteins (low density)</subject><subject>Lipoproteins, LDL - blood</subject><subject>Low density lipoprotein</subject><subject>Male</subject><subject>Males</subject><subject>Medicine and Health Sciences</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Neuropeptide Y</subject><subject>Neuropeptide Y - genetics</subject><subject>Neuropeptide Y - metabolism</subject><subject>Neuropeptides</subject><subject>Nutrition research</subject><subject>Patients</subject><subject>Phenotypes</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Population</subject><subject>Promoter Regions, Genetic</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Research and Analysis Methods</subject><subject>Restriction fragment length polymorphism</subject><subject>Risk</subject><subject>Risk management</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Satiety</subject><subject>Science</subject><subject>Transcription</subject><subject>Triglycerides - blood</subject><subject>Zoology</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNks1u1DAUhSMEoqXwBggssZlKpPgntuMNUhmgRBqVWZRFV5aT3HQ8ZOzUTkB9Ax6bhEmrFrFg5Sv7nO9eX50keUnwCWGSvNv6ITjTnnTewQkmIsuYfJQcEsVoKihmj-_VB8mzGLcYc5YL8TQ5oFJmSpHsMPl1GqOvrOmtd8g36ByG4DvoeltDeokW5-vLY2RcjQrXQ2hh-G5dSkroDVoUK_Lh-C06A-f7mw7S9Wau0NKHAO0eOpnXrYk7g1a2s3VEP22_QReToyjQR2tGGsTnyZPGtBFezOdR8u3zp4vll3T19axYnq7SinPVp7KqweCGiLyuTSaYqg3BuVSgMKUZJw1UQkjGS5wbTjmpSgZQ5oywimEpKTtKXu-5XeujnpcYNcmpkgJLwUZFsVfU3mx1F-zOhBvtjdV_Lny40ib0tmpBlyXPCSvLTFCT0bGZVJKWsiFKNEJyMbLez92Gcgd1Ba4Ppn0Affji7EZf-R-aYyGUlCNgMQOCvx4g9npnYwVtaxz4YZqbSTYugNP_kfIxJBmZvvjmL-m_F5HtVVXwMQZo7uYmWE8ZvHXpKYN6zuBoe3X_z3em29Cx3_XE2Mc</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Patel, Roma</creator><creator>Dwivedi, Mitesh</creator><creator>Mansuri, Mohmmad Shoab</creator><creator>Ansarullah</creator><creator>Laddha, Naresh C</creator><creator>Thakker, Ami</creator><creator>Ramachandran, A V</creator><creator>Begum, Rasheedunnisa</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20161001</creationdate><title>Association of Neuropeptide-Y (NPY) and Interleukin-1beta (IL1B), Genotype-Phenotype Correlation and Plasma Lipids with Type-II Diabetes</title><author>Patel, Roma ; Dwivedi, Mitesh ; Mansuri, Mohmmad Shoab ; Ansarullah ; Laddha, Naresh C ; Thakker, Ami ; Ramachandran, A V ; Begum, Rasheedunnisa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559t-7cdea0f168dda4639da10879e9022451fec66735b08a5251cb3eeb8313c307723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Alleles</topic><topic>Beta cells</topic><topic>Biochemistry</topic><topic>Biology and Life Sciences</topic><topic>Blood Glucose - analysis</topic><topic>Body mass</topic><topic>Body Mass Index</topic><topic>Body weight</topic><topic>Cardiovascular disease</topic><topic>Case-Control Studies</topic><topic>Cholesterol</topic><topic>Correlation</topic><topic>Cytokines</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetic retinopathy</topic><topic>DNA</topic><topic>Energy balance</topic><topic>Exons</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Gene polymorphism</topic><topic>Genetic Association Studies</topic><topic>Genotype</topic><topic>Genotyping</topic><topic>Haplotypes</topic><topic>Health risks</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Interleukin</topic><topic>Interleukin 1</topic><topic>Interleukin-1beta - genetics</topic><topic>Interleukin-1beta - metabolism</topic><topic>Linkage analysis</topic><topic>Linkage Disequilibrium</topic><topic>Lipid metabolism</topic><topic>Lipids</topic><topic>Lipids - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Patel, Roma</au><au>Dwivedi, Mitesh</au><au>Mansuri, Mohmmad Shoab</au><au>Ansarullah</au><au>Laddha, Naresh C</au><au>Thakker, Ami</au><au>Ramachandran, A V</au><au>Begum, Rasheedunnisa</au><au>Grolmusz, Vince</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of Neuropeptide-Y (NPY) and Interleukin-1beta (IL1B), Genotype-Phenotype Correlation and Plasma Lipids with Type-II Diabetes</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>11</volume><issue>10</issue><spage>e0164437</spage><epage>e0164437</epage><pages>e0164437-e0164437</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Neuropeptide Y (NPY) is known to play a role in the regulation of satiety, energy balance, body weight, and insulin release. Interleukin-1beta (IL1B) has been associated with loss of beta-cell mass in type-II diabetes (TIID).
The present study attempts to investigate the association of NPY exon2 +1128 T/C (Leu7Pro; rs16139), NPY promoter -399 T/C (rs16147) and IL1B -511 C/T (rs16944) polymorphisms with TIID and their correlation with plasma lipid levels, BMI, and IL1B transcript levels.
PCR-RFLP was used for genotyping these polymorphisms in a case-control study involving 558 TIID patients and 1085 healthy age-matched controls from Gujarat. Linkage disequilibrium and haplotype analysis of the NPY polymorphic sites were performed to assess their association with TIID. IL1B transcript levels in PBMCs were also assessed in 108 controls and 101 patients using real-time PCR.
Our results show significant association of both structural and promoter polymorphisms of NPY (p<0.0001 and p<0.0001 respectively) in patients with TIID. However, the IL1B C/T polymorphism did not show any association (p = 0.3797) with TIID patients. Haplotype analysis revealed more frequent association of CC and CT haplotypes (p = 3.34 x 10-5, p = 6.04 x 10-9) in diabetics compared to controls and increased the risk of diabetes by 3.02 and 2.088 respectively. Transcript levels of IL1B were significantly higher (p<0.0001) in patients as compared to controls. Genotype-phenotype correlation of IL1B polymorphism did not show any association with its higher transcript levels. In addition, NPY +1128 T/C polymorphism was found to be associated with increased plasma LDL levels (p = 0.01).
The present study provides an evidence for a strong correlation between structural and promoter polymorphisms of NPY gene and upregulation of IL1B transcript levels with susceptibility to TIID and altering the lipid metabolism in Gujarat population.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27749914</pmid><doi>10.1371/journal.pone.0164437</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-10, Vol.11 (10), p.e0164437-e0164437 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1829760763 |
| source | PubMed Central (Open Access); Publicly Available Content Database |
| subjects | Adult Alleles Beta cells Biochemistry Biology and Life Sciences Blood Glucose - analysis Body mass Body Mass Index Body weight Cardiovascular disease Case-Control Studies Cholesterol Correlation Cytokines Deoxyribonucleic acid Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - pathology Diabetic retinopathy DNA Energy balance Exons Female Gene Frequency Gene polymorphism Genetic Association Studies Genotype Genotyping Haplotypes Health risks Humans Insulin Insulin resistance Interleukin Interleukin 1 Interleukin-1beta - genetics Interleukin-1beta - metabolism Linkage analysis Linkage Disequilibrium Lipid metabolism Lipids Lipids - blood Lipoproteins Lipoproteins (low density) Lipoproteins, LDL - blood Low density lipoprotein Male Males Medicine and Health Sciences Metabolism Middle Aged Neuropeptide Y Neuropeptide Y - genetics Neuropeptide Y - metabolism Neuropeptides Nutrition research Patients Phenotypes Polymerase chain reaction Polymorphism Polymorphism, Single Nucleotide Population Promoter Regions, Genetic Real-Time Polymerase Chain Reaction Research and Analysis Methods Restriction fragment length polymorphism Risk Risk management RNA, Messenger - metabolism Rodents Satiety Science Transcription Triglycerides - blood Zoology |
| title | Association of Neuropeptide-Y (NPY) and Interleukin-1beta (IL1B), Genotype-Phenotype Correlation and Plasma Lipids with Type-II Diabetes |
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