Retinoid Metabolism and Diabetes Mellitus

Abstract

Retinoid acid is a metabolite of vitamin A and functions as an important factor in cell survival, differentiation and death. Most previous studies on retinoid metabolism have focused on its association with cancer, hematologic and dermatologic disorders. Given the special concern over the recent increase in the prevalence of diabetes worldwide, the role of retinoid metabolism on glucose metabolism and insulin resistance in the human body is of marked importance. Therefore, in this issue, we review the literature on the association of retinoid metabolism with glucose tolerance, with regard to insulin secretion, pancreatic autoimmunity, insulin sensitivity and lipid metabolism. Further, we tried to assess the possibility of using retinoids as a novel therapeutic strategy for diabetes.

Prepartum vitamin A supplementation enhances goat doe health status and kid viability and performance

“…In addition, we showed , 2000, , Blumentrath et al 2001Xiao and Song, 2013). They can also increase insulin secretion and sensitivity (Driscoll et al 1997, Rhee andPlutzky, 2012). All of these have important role in lipogenesis and cholesterol synthesis.…”

Quantitative Proteomic and Functional Analysis of Liver Mitochondria from High Fat Diet (HFD) Diabetic Mice

“…Retinyl esters, retinol, retinal, retinoic acid, and oxidized and conjugated metabolites of both retinol and retinoic acid are different forms of retinoids, and they are critical for development of the nervous system and notochord and many other embryonic structures, as well as for cell proliferation and differentiation (61). Retinoids have also been known to play an important role in glucose and lipid metabolism by regulating gene expression (62,63). All-trans-retinoid acid (at-RA) functions as a ligand for nuclear retinoid acid receptor and they heterodimerize with PPARs, the main players in lipid and glucose metabolism, and thus the effects of retinoids on insulin sensitivity is thought to be through dimerization with PPAR␥.…”

Deriving at candidate genes of metabolic stress from pancreas of WNIN/GR-Ob mutant rats

“…These observation are important since Obesity/T2D is viewed as a state of profound stress and inflammation and with Mutants exacerbating these changes. 1,2,5,33 Emerging reports suggest the role of epigenetic modifications in obesity and diabetes. Global and local epigenomic markers can be used as the therapeutic targets for metabolic disease prevention Overrepresented Gene Ontology/KEGG Pathway annotations were significant at p < 0.05.…”

“…32 Nfyb, a transcription factor which promotes basal transcription of rat pyruvate carboxylase gene in β-cells, also showed an increase in the present study, and the mechanism needs to be understood. Retinoic Acid (RA) well characterized differentiation agent is known to improve pancreatic β-cells function in the following ways: (1) facilitating glucose stimulated insulin release in vitamin A depleted rats, 33 (2) induces biphasic glucose stimulated insulin secretion in human fetal pancreas explants, 33 (3) enhances insulin production in insulin secreting cell lines, 33 (4) increases glucokinase activity and gene expression levels in primary rat islets culture and insulinoma cell lines. 33 In fact we have demonstrated for (array analysis) downregulation in several genes in mutants involved in retinol metabolic pathway (Dhrs3, Cyp2a1, RPE65 DGAT2, Ugt1a, Cyp2b21, Ugt2b5, rdh11, Cyp2b12, and Cyb2b2) signifying a functional role of this pathway in metabolic disorder/obesity in the pancreas of these rats (Table 1E).…”