Explore chapters and articles related to this topic
Collodion baby and harlequin ichthyosis
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
D. V. Lakshmi, Sahana M. Srinivas
The collodion membrane occurs due to a genetic defect in epidermal cornification, keratinocyte protein, and lipid metabolism. Autosomal recessive congenital ichthyosis (ARCI) and nonbullous congenital ichthyosiform erythroderma are seen in the majority of infants due to a defect in the transglutaminase 1 gene (TGM1) mutation localized on chromosome 14q11 [4]. Moreover, five different gene localizations have been detected in ARCI. Lipoxygenases gene (ALOX 12B, ALOXE3), ATP-binding cassette transporter (ABCA12), and ichthyin receptor and a cytochrome p450 family member FLJ39501 are the newer genes detected. Approximately 80% of ARCI is due to involvement of these six genes [5–9].
Physiological and pathophysiological roles of hepoxilins and their analogs
Published in Drug Metabolism Reviews, 2023
Sara A. Helal, Fadumo Ahmed Isse, Samar H. Gerges, Ayman O. S. El-Kadi
Even though HXs mainly are produced from 12S-LOX, a novel LOX pathway in the normal epidermis was proposed in 2002 by Fischer and his colleagues who provided genetic evidence that established the role of LOX enzymes in the skin (Jobard et al. 2002). The analysis of the catalytic activities of 12 R-LOX and eLOX3 in the skin suggested that they can form HX metabolites (Brash et al. 2007). In addition, biochemical studies using recombinant enzymes found that the biochemical activities of the eLOX3 enzyme exhibit hydroperoxide isomerase activity and can convert 12 R-HpETE to specific hepoxilin-type derivatives (Yu et al. 2003). Genetic mutations of either arachidonate 12-lipoxygenase gene (ALOX12B) which encodes 12 R-LOX enzyme or arachidonate lipoxygenase-3 gene (ALOXE3) encoding eLOX3 enzyme result in deficiency of some HXs and can cause loss of the integrity of the epidermal water barrier. This is greatly associated with a skin disease called ichthyosis which is characterized by severe dehydration, infections, and chronic blistering of the skin (Muñoz-Garcia et al. 2014).
Activation of ectopic olfactory receptor 544 induces GLP-1 secretion and regulates gut inflammation
Published in Gut Microbes, 2021
Chunyan Wu, Mi-Young Jeong, Jung Yeon Kim, Giljae Lee, Ji-Sun Kim, Yu Eun Cheong, Hyena Kang, Chung Hwan Cho, Jimin Kim, Min Kyung Park, You Kyoung Shin, Kyoung Heon Kim, Geun Hee Seol, Seung Hoi Koo, GwangPyo Ko, Sung-Joon Lee
Trehalose is a functional disaccharide with several metabolic functions, such as suppression of inflammatory responses.48,49 The anti-obesity effect of trehalose has been reported. Trehalose suppressed adipocyte hypertrophy and alleviation of impaired glucose tolerance.50 In addition, oral administration of trehalose reportedly induces beige adipogenesis and thermogenesis and reduces white adipocyte size; thus, trehalose is considered a thermogenic dietary compound.51 Trehalose also induces antioxidative and lysosomal gene expression, resulting in reduced cellular reactive oxygen species in adipose tissues.52 In addition, trehalose has been shown to activate hepatic Aloxe3, which results in the reduction of weight gain and hepatic steatosis, thus ameliorating metabolic disease.53 These results collectively indicate that trehalose may have anti-obesogenic effects in multiple organs after uptake by the intestine.
Transcriptional control and transcriptomic analysis of lipid metabolism in skin barrier formation and atopic dermatitis (AD)
Published in Expert Review of Proteomics, 2019
Nilika Bhattacharya, Gitali Ganguli-Indra, Arup K. Indra
In addition to the enzymes mentioned above, western blot analysis showed subsequent reduction in the protein levels of LASS2, GBA2, and epidermis-type lipoxygenase 3 (eLOX3) in Ctip2−/- skin compared with wild-type skin by 1-fold, 0.6-fold, and 0.8-fold, respectively. In vivo ChIP assay was performed to determine which of the genes involved in lipid metabolism are direct targets of the TF CTIP2. The results also showed that Lass2, Gba2, and Aloxe3 are possible direct targets of CTIP2 in the regulation of skin lipid metabolism by direct recruitment of the TF to the promoter region of those genes. The above results obtained from RT-qPCR analysis and in-vivo ChIP assay were indicative of the fact that the expression of a subset of genes encoding enzymes involved in the sphingolipid biosynthesis pathways get altered during skin organogenesis in the absence of CTIP2 and therefore is under direct or indirect regulation by CTIP2 [23].