TY - JOUR
T1 - Deep multi-OMICs and multi-tissue characterization in a pre-and postprandial state in human volunteers
T2 - The GEMM family study research design
AU - Bastarrachea, Raul A.
AU - Laviada-Molina, Hugo A.
AU - Nava-Gonzalez, Edna J.
AU - Leal-Berumen, Irene
AU - Escudero-Lourdes, Claudia
AU - Escalante-Araiza, Fabiola
AU - Peschard, Vanessa Giselle
AU - Veloz-Garza, Rosa A.
AU - Haack, Karin
AU - Martínez-Hernández, Angélica
AU - Barajas-Olmos, Francisco M.
AU - Molina-Segui, Fernanda
AU - Buenfil-Rello, Fatima A.
AU - Gonzalez-Ramirez, Lucia
AU - Janssen-Aguilar, Reinhard
AU - Lopez-Muñoz, Ricardo
AU - Perez-Cetina, Fernanda
AU - Gaytan-Saucedo, Janeth F.
AU - Vaquera, Zoila
AU - Cornejo-Barrera, Judith
AU - Castillo-Pineda, Juan Carlos
AU - Murillo-Ramirez, Areli
AU - Diaz-Tena, Sara P.
AU - Figueroa-Nuñez, Benigno
AU - González-López, Laura
AU - Salinas-Osornio, Rocío A.
AU - Valencia-Rendón, Melesio E.
AU - Ángeles-Chimal, José
AU - Tapia, Jesús Santa Olalla
AU - Remes-Troche, José M.
AU - Valdovinos-Chavez, Salvador B.
AU - Huerta-Avila, Eira E.
AU - Han, Xianlin
AU - Orozco, Lorena
AU - Rodriguez-Ayala, Ernesto
AU - Weintraub, Susan
AU - Gallegos-Cabrales, Esther C.
AU - Cole, Shelley A.
AU - Kent, Jack W.
N1 - Publisher Copyright:
© 2018 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2018/11/2
Y1 - 2018/11/2
N2 - Cardiovascular disease (CVD) and type 2 diabetes (T2D) are increasing worldwide. This is mainly due to an unhealthy nutrition, implying that variation in CVD risk may be due to variation in the capacity to manage a nutritional load. We examined the genomic basis of postprandial metabolism. Our main purpose was to introduce the GEMM Family Study (Genetics of Metabolic Diseases in Mexico) as a multi-center study carrying out an ongoing recruitment of healthy urban adults. Each participant received a mixed meal challenge and provided a 5-hours’ time course series of blood, buffy coat specimens for DNA isolation, and adipose tissue (ADT)/skeletal muscle (SKM) biopsies at fasting and 3 h after the meal. A comprehensive profiling, including metabolomic signatures in blood and transcriptomic and proteomic profiling in SKM and ADT, was performed to describe tendencies for variation in postprandial response. Our data generation methods showed preliminary trends indicating that by characterizing the dynamic properties of biomarkers with metabolic activity and analyzing multi-OMICS data it could be possible, with this methodology and research design, to identify early trends for molecular biology systems and genes involved in the fasted and fed states.
AB - Cardiovascular disease (CVD) and type 2 diabetes (T2D) are increasing worldwide. This is mainly due to an unhealthy nutrition, implying that variation in CVD risk may be due to variation in the capacity to manage a nutritional load. We examined the genomic basis of postprandial metabolism. Our main purpose was to introduce the GEMM Family Study (Genetics of Metabolic Diseases in Mexico) as a multi-center study carrying out an ongoing recruitment of healthy urban adults. Each participant received a mixed meal challenge and provided a 5-hours’ time course series of blood, buffy coat specimens for DNA isolation, and adipose tissue (ADT)/skeletal muscle (SKM) biopsies at fasting and 3 h after the meal. A comprehensive profiling, including metabolomic signatures in blood and transcriptomic and proteomic profiling in SKM and ADT, was performed to describe tendencies for variation in postprandial response. Our data generation methods showed preliminary trends indicating that by characterizing the dynamic properties of biomarkers with metabolic activity and analyzing multi-OMICS data it could be possible, with this methodology and research design, to identify early trends for molecular biology systems and genes involved in the fasted and fed states.
KW - Gemm family study
KW - Mixed meal challenge
KW - Multi-OMICs
KW - Postprandial metabolism
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U2 - 10.3390/genes9110532
DO - 10.3390/genes9110532
M3 - Article
C2 - 30400254
AN - SCOPUS:85056579145
SN - 2073-4425
VL - 9
JO - Genes
JF - Genes
IS - 11
M1 - 532
ER -