Diabetes susceptibility in Mayas: Evidence for the involvement of polymorphisms in HHEX, HNF4α, KCNJ11, PPARγ, CDKN2A/2B, SLC30A8, CDC123/CAMK1D, TCF7L2, ABCA1 and SLC16A11 genes

Lara-Riegos, Julio; Ortiz-López, Marı́a Guadalupe; Peña-Espinoza, Barbara Itzel; Montúfar-Robles, Isela; Peña‐Rico, M. A.; Sánchez-Pozos, Katy; Granados-Silvestre, M. A.; Márta, Mészáros

doi:10.1016/j.gene.2015.03.065

Cited by 60 publications

(52 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Villarreal‐Molina et al, who analyzed Mexican individuals aged 20 to 69 years, identified an association between rs9282541 in the ABCA1 gene in a dominant model of risk and early‐onset T2D (OR: 2.75; P = 9.4E−8), and this association was somewhat lower in the later‐onset forms (OR: 1.82; P = .010) . Similar findings were reported by Lara‐Riegos et al in Mayas (OR: 2.29; 95% CI: 1.33‐3.92, P = .003); however, this study did not consider the age of presentation in the analysis . In contrast to these results, Campbell et al did not identify an association for this variant in adults of Native American ancestry from Colombia .…”

Section: Discussionsupporting

confidence: 64%

Associations of common variants in the SLC16A11 , TCF7L2, and ABCA1 genes with pediatric-onset type 2 diabetes and related glycemic traits in families: A case-control and case-parent trio study

et al. 2017

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 64%

Associations of common variants in the SLC16A11 , TCF7L2, and ABCA1 genes with pediatric-onset type 2 diabetes and related glycemic traits in families: A case-control and case-parent trio study

et al. 2017

View full text Add to dashboard Cite

show abstract

“…The CDKN2A/B locus, at chromosome 9p21, influences diabetes risk across varied ethnicities and geography [1–3], including people of European [4–9], Asian [10–24], Indian [25], Pakistani [26], Mexican [27–29] and Arab [30–32] descent. CDKN2A/B polymorphisms impact risk of gestational diabetes [33–35], early progression to type 2 diabetes after gestational diabetes [36], post-transplant diabetes [37, 38] and cystic fibrosis-related diabetes [39].…”

Section: The Cdkn2a/b Locus Impacts Human Diabetes Riskmentioning

confidence: 99%

Islet biology, the CDKN2A/B locus and type 2 diabetes risk

et al. 2016

View full text Add to dashboard Cite

Type 2 diabetes, fuelled by the obesity epidemic, is an escalating worldwide cause of personal hardship and public cost. Diabetes incidence increases with age, and many studies link the classic senescence and ageing protein p16INK4A to diabetes pathophysiology via pancreatic islet biology. Genome-wide association studies (GWASs) have unequivocally linked the CDKN2A/B locus, which encodes p16 inhibitor of cyclin-dependent kinase (p16INK4A) and three other gene products, p14 alternate reading frame (p14ARF), p15INK4B and antisense non-coding RNA in the INK4 locus (ANRIL), with human diabetes risk. However, the mechanism by which the CDKN2A/B locus influences diabetes risk remains uncertain. Here, we weigh the evidence that CDKN2A/B polymorphisms impact metabolic health via islet biology vs effects in other tissues. Structured in a bedside-to-bench-to-bedside approach, we begin with a summary of the evidence that the CDKN2A/B locus impacts diabetes risk and a brief review of the basic biology of CDKN2A/B gene products. The main emphasis of this work is an in-depth look at the nuanced roles that CDKN2A/B gene products and related proteins play in the regulation of beta cell mass, proliferation and insulin secretory function, as well as roles in other metabolic tissues. We finish with a synthesis of basic biology and clinical observations, incorporating human physiology data. We conclude that it is likely that the CDKN2A/B locus influences diabetes risk through both islet and non-islet mechanisms.

show abstract

“…For example, Lara-Riegos et al found T2D susceptibility in Mexican Mestizos was associated with a loss-of-function mutation in ABCA1; 20 however, genetic variation in ABCA1 was not found to predict T2D in other populations. 21 Moreover, mutation in genes for ApoA1, CETP, SR-B1, and Niemann-Pick disease, type C1 (NPC1) tend to increase a carrier's risk for T2D.…”

Section: New Aspects Of Cellular Cholesterol Regulation On Blood Glucmentioning

confidence: 99%

New Aspects of Cellular Cholesterol Regulation on Blood Glucose Control—Review and Perspective on the Impact of Statin Medications on Metabolic Health

Grice

Elmendorf

2017

US Endocrinology

View full text Add to dashboard Cite

Cholesterol is an essential component of cell membranes, and during the past several years, diabetes researchers have found that membrane cholesterol levels in adipocytes, skeletal muscle fibers and pancreatic beta cells influence insulin action and insulin secretion. Consequently, it is thought that dysregulated cell cholesterol homeostasis could represent a determinant of type 2 diabetes (T2D). Recent clinical findings compellingly add to this notion by finding increased T2D susceptibility in individuals with alterations in a variety of cholesterol metabolism genes. While it remains imperfectly understood how statins influence glucose metabolism, the fact that they display an influence on blood glucose levels and diabetes susceptibility seems to intensify the emerging importance of understanding cellular cholesterol in glucose metabolism. Taking this into account, this review first presents cell system and animal model findings that demonstrate the negative impact of cellular cholesterol accumulation or diminution on insulin action and insulin secretion. With this framework, a description of how changes in cholesterol metabolism genes are associated with T2D susceptibility will be presented. In addition, the connection between statins and T2D risk will be reviewed with expanded information on pitavastatin, a newer statin medication that displays actions favoring metabolic health.

show abstract

Diabetes susceptibility in Mayas: Evidence for the involvement of polymorphisms in HHEX, HNF4α, KCNJ11, PPARγ, CDKN2A/2B, SLC30A8, CDC123/CAMK1D, TCF7L2, ABCA1 and SLC16A11 genes

Cited by 60 publications

References 49 publications

Associations of common variants in the SLC16A11 , TCF7L2, and ABCA1 genes with pediatric-onset type 2 diabetes and related glycemic traits in families: A case-control and case-parent trio study

Associations of common variants in the SLC16A11 , TCF7L2, and ABCA1 genes with pediatric-onset type 2 diabetes and related glycemic traits in families: A case-control and case-parent trio study

Islet biology, the CDKN2A/B locus and type 2 diabetes risk

New Aspects of Cellular Cholesterol Regulation on Blood Glucose Control—Review and Perspective on the Impact of Statin Medications on Metabolic Health

Contact Info

Product

Resources

About