The<i>aristaless</i>-like homeobox protein Alx3 as an etiopathogenic factor for diabetes mellitus

Vallejo, Mario

doi:10.4161/isl.3.2.14658

Cited by 2 publications

(2 citation statements)

References 23 publications

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“…Thus, unrecognized metabolic perturbations may be present in more models than currently appreciated. A prominent example is the Alx3 transcription factor, which, independent of its role in cranial mesenchyme, is required for insulin secretion and glucose homeostasis in the adult [Mirasierra et al, 2011; Vallejo, 2011]. Studying NTD models for metabolic defects would not only have implications for a better understanding of the cause of neural tube defects and their prevention, but could also reveal novel roles for developmental genes in adult physiology.…”

Section: Mechanisms and Mouse Models: Nutrient Modulation Of Neural Tmentioning

confidence: 99%

Modeling anterior development in mice: Diet as modulator of risk for neural tube defects

Kappen¹

2013

American J of Med Genetics Pt C

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Head morphogenesis is a complex process that is controlled by multiple signaling centers. The most common defects of cranial development are craniofacial defects, such as cleft lip and cleft palate, and neural tube defects, such as anencephaly and encephalocoele in humans. More than 400 genes that contribute to proper neural tube closure have been identified in experimental animals, but only very few causative gene mutations have been identified in humans, supporting the notion that environmental influences are critical. The intrauterine environment is influenced by maternal nutrition, and hence, maternal diet can modulate the risk for cranial and neural tube defects. This article reviews recent progress toward a better understanding of nutrients during pregnancy, with particular focus on mouse models for defective neural tube closure. At least four major patterns of nutrient responses are apparent, suggesting that multiple pathways are involved in the response, and likely in the underlying pathogenesis of the defects. Folic acid has been the most widely studied nutrient, and the diverse responses of the mouse models to folic acid supplementation indicate that folic acid is not universally beneficial, but that the effect is dependent on genetic configuration. If this is the case for other nutrients as well, efforts to prevent neural tube defects with nutritional supplementation may need to become more specifically targeted than previously appreciated. Mouse models are indispensable for a better understanding of nutrient–gene interactions in normal pregnancies, as well as in those affected by metabolic diseases, such as diabetes and obesity.

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Section: Mechanisms and Mouse Models: Nutrient Modulation Of Neural Tmentioning

confidence: 99%

Modeling anterior development in mice: Diet as modulator of risk for neural tube defects

Kappen¹

2013

American J of Med Genetics Pt C

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“…In humans, mutations in ALX3 gene result in severe neurological disorder associated to genital malformation, and pancreatic defects in 2 of the most severe cases. In human, mutations in ALX4 gene are associated with defects in skull and craniofacial development; this gene was found in one of several loci linked to high risk for type 2 diabetes identified in a genome‐wide association study (Vallejo, ).…”

Section: Hox Genes and Metabolic Processesmentioning

confidence: 99%

The HOX genes network in metabolic diseases

Procino

Cillo

2013

Cell Biology International

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Fat distribution is associated with metabolic risk. Differences in cellular characteristics and metabolic functions of these depots have been described, but the molecular mechanisms involved are not understood. The pathogenesis and pathophysiology of metabolic disease can be better understood by studying the molecular mechanisms that control the development and function of adipose tissue (adipogenesis). Homeobox genes are transcription factors that act during normal development and contain the homeobox, a 183bp DNA sequence coding for a 61 amino acid domain defined as homeodomain (HD). Class 1 homeobox genes (Hox genes) have a critical role in controlling positional information and tissue patterning during development. The expression of the whole HOX gene network in different deposits of normal adult human white adipose tissue (intraperitoneal, extra-peritoneal and dermis) indicate a marked expression in adipose tissue. Furthermore, this expression seems to vary in different bodily deposits of white adipose tissue and between white and brown adipose tissue. The purpose of this mini-review is to discuss the role of HOX genes in metabolic diseases.

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Thearistaless-like homeobox protein Alx3 as an etiopathogenic factor for diabetes mellitus

Abstract: To cite this article: Mario Vallejo (2011) The aristaless-like homeobox protein Alx3 as an etiopathogenic factor for diabetes mellitus, Islets, 3:2, 66-68,

Cited by 2 publications

References 23 publications

Modeling anterior development in mice: Diet as modulator of risk for neural tube defects

Modeling anterior development in mice: Diet as modulator of risk for neural tube defects

The HOX genes network in metabolic diseases

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