Common variant in MTNR1B associated with increased risk of type 2 diabetes and impaired early insulin secretion

By V. Lyssenko, C. Nagorny, M. Erdos, N. Wierup, A. Jonsson, P. Spégel, M. Bugliani, R. Saxena, M. Fex, N. Pulizzi and 15 more. Nature Genetics, 2009

777 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/121226213735df75983c9fd47cc04dd05bdb916a

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In Endocrine and Autonomic Systems

1. U. Albrecht
2. C. Dibner
3. D. Cardinali
4. F. B. Hu
5. U. Schibler
6. J. Takahashi
7. J. Bass
8. Luigi Fontana

In Nutrition and Dietetics

1. James B. Meigs
2. F. B. Hu
3. Qi Sun
4. U. Albrecht
5. W. Willett
6. D. Mozaffarian
7. F. B. Hu
8. G. Hoffmann

Citations in the corpus

• International Union of Basic and Clinical Pharmacology. LXXV. Nomenclature, Classification, and Pharmacology of G Protein-Coupled Melatonin Receptors (2010, background): “sons with genetic variations in the MTNR1B gene encoding the MT2 melatonin receptor (Bouatia-Naji et al., 2009; Lyssenko et al., 2009; Prokopenko et al., 2009).”
• Human genetic variation and its contribution to complex traits (2009, background): “For example, the genetic propensity to develop type 2 diabetes (T2D) seems to involve genes in several different pathways that affect pancreatic β-cell formation and function, as well as pathways affecting fasting glucose levels and obesit”
• Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes (2012, neutral): “However the inhibitory effect is consistent in replicated experiments with clonal β-cells [227, 229, 233, 234].”
• Melatonin--a pleiotropic, orchestrating regulator molecule. (2011, background): “The human MT2 polymorphisms associated with increased risk for developing diabetes type 2 (Staiger et al., 2008; Bouatia-Naji et al., 2009; Lyssenko et al., 2009; Shieh et al., 2009; Sparsø et al., 2009; Liu et al., 2010) may be interpreted in this context.”
• The mammalian circadian timing system: organization and coordination of central and peripheral clocks. (2010, background): “Genetic studies in humans have revealed a possible link between MTNR1B allele variants and hyperglycemia, impaired earlyphase insulin secretion, and β-cell function (258, 259).”
• Pathogenesis of Type 2 Diabetes Mellitus (2015, neutral): “A great number of studies have suggested that genetic variants in or near KCNJ11, TCF7L2, WFS1, HNF1B, IGF2BP2, CDKN2ACDKN2B, CDKAL1, SLC30A8, HHEX/IDE, KCNQ1, THADA, TSPAN8/ LGR5, DC123/CAMK1D, JAZF1, MTNR1B, DGKB/TMEM195, GCK, PROX1, ADCY5, SRR, CENTD2, ST6GAL1, HNF4A, KCNK16, FITM2-R3HDML-HNF4A, ”
• Adverse metabolic and cardiovascular consequences of circadian misalignment (2009, background): “Recent evidence in humans of increased risk for type 2 diabetes in a genetic variant of melatonin 1B receptor (Mel1B), expression of Mel1B in pancreatic -cells, and inhibition of glucose-induced insulin release by melatonin (38, 39), raises the possibility that the reversal of the melatonin profile ”
• Twelve type 2 diabetes susceptibility loci identified through large-scale association analysis (2010, background): “…of estimates of parent-of-origin–specific effect sizes observed at the KCNQ1 and KLF14 signals and at a recently described locus on chromosome 11p15 (which confers substantial risk when paternally inherited but is protective when maternally transmitted 11 ), this figure rises to ~1.16.”