Редактирование: CIDEA

Cell death activator CIDE-A (Cell death-inducing DFFA-like effector A)

==Publications==

{{medline-entry
|title=Growth hormone receptor expression in human gluteal versus abdominal subcutaneous adipose tissue: Association with body shape.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27015877
|abstract=Growth hormone (GH) administration reduces abdominal, but not lower body, fat mass. To gain insight into the underlying mechanisms, this study examined the expression of the GH receptor ([[GHR]]) and some of its targets in abdominal and gluteal adipose tissue. [[GHR]] and GH targets in the lipolytic pathway were assessed (quantitative PCR/Western blotting) in adipose aspirates from premenopausal women [n = 15, age 26.9 ± 6.1 years, body mass index (BMI) 28.0 ± 6.8 kg/m(2) ] and men (n = 28, age 29.2 ± 7.0 years, BMI 26.9 ± 3.7 kg/m(2) ). [[GHR]] mRNA expression was lower in the gluteal depot when compared with the abdominal depot (P = 0.01). Abdominal [[GHR]] correlated negatively with age and BMI, whereas gluteal [[GHR]] was associated with lower waist-to-hip ratio (WHR), that is, pear shape. In both sites, [[GHR]] mRNA correlated strongly with genes important for the regulation of lipolysis: adipose tissue triglyceride lipase (ATGL), hormone-sensitive lipase, perilipin, and [[CIDEA]] (all P < 0.001), independently of BMI, WHR, age, and sex. [[GHR]] protein was lower in the gluteal fat when compared with the abdominal fat (P = 0.03) and correlated with ATGL protein in the gluteal depot (P < 0.001). [[GHR]] levels correlate with levels of lipases and lipid droplet-associated proteins crucial for lipolysis. Thus, higher [[GHR]] expression in the abdominal depot when compared with the gluteal depot may underlie the in vivo effect of GH to specifically reduce abdominal adipose tissue mass.
|mesh-terms=* Adipose Tissue
* Adiposity
* Adult
* Aging
* Body Mass Index
* Buttocks
* Carrier Proteins
* Female
* Gene Expression
* Human Growth Hormone
* Humans
* Lipase
* Lipolysis
* Male
* Obesity
* Premenopause
* RNA, Messenger
* Receptors, Somatotropin
* Subcutaneous Fat, Abdominal
* Waist-Hip Ratio

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5084456
}}
{{medline-entry
|title=The developmental transition of ovine adipose tissue through early life.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23351024
|abstract=Hypothermia induced by cold exposure at birth is prevented in sheep by the rapid onset of non-shivering thermogenesis in brown adipose tissue (BAT). Changes in adipose tissue composition in early life are therefore essential for survival but also influence adiposity in later life and were thus examined in detail during early development. Changes in adipose composition were investigated by immunohistochemistry and qRT-PCR between the period from the first appearance of adipose in the mid gestation foetus, through birth and up to 1 month of age. We identified four distinct phases of development, each associated with pronounced changes in tissue histology and in distribution of the BAT specific uncoupling protein (UCP)1. At mid gestation, perirenal adipose tissue exhibited a dense proliferative, structure marked by high expression of KI-67 but with no [[UCP1]] or visible lipid droplets. By late gestation large quantities of [[UCP1]] were present, lipid storage was evident and expression of BAT-related genes were abundant (e.g. prolactin and β3 receptors). Subsequently, within 12 h of birth, the depot was largely depleted of lipid and expression of genes such as [[UCP1]], PGC1α, [[CIDEA]] peaked. By 30 days [[UCP1]] was undetectable and the depot contained large lipid droplets; however, genes characteristic of BAT (e.g. [[PRDM16]] and BMP7) and most characteristic of white adipose tissue (e.g. leptin and RIP140) were still abundant. Adipose tissue undergoes profound compositional changes in early life, of which an increased understanding could offer potential interventions to retain BAT in later life.
|mesh-terms=* Adipose Tissue, Brown
* Adiposity
* Aging
* Animals
* Lipid Metabolism
* Sheep
|keywords=* brown
* uncoupling protein
* white
|full-text-url=https://sci-hub.do/10.1111/apha.12053
}}
{{medline-entry
|title=Relations of adipose tissue [[CIDEA]] gene expression to basal metabolic rate, energy restriction, and obesity: population-based and dietary intervention studies.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17895319
|abstract=Cell death-inducing DNA fragmentation factor-alpha-like effector A ([[CIDEA]]) could be a potential target for the treatment of obesity via the modulation of metabolic rate, based on the findings that [[CIDEA]] inhibits the brown adipose tissue uncoupling process in rodents. Our objects were to investigate the putative link between [[CIDEA]] and basal metabolic rate in humans and to elucidate further the role of [[CIDEA]] in human obesity. We have explored [[CIDEA]] gene expression in adipose tissue in two different human studies: a cross-sectional and population-based study assessing body composition and metabolic rate (Mölndal Metabolic study, n = 92); and a longitudinal intervention study of obese subjects treated with a very low calorie diet (VLCD) (VLCD study, n = 24). The [[CIDEA]] gene was predominantly expressed in adipocytes as compared with other human tissues. [[CIDEA]] gene expression in adipose tissue was inversely associated with basal metabolic rate independently of body composition, age, and gender (P = 0.014). The VLCD induced an increase in adipose tissue [[CIDEA]] expression (P < 0.0001) with a subsequent decrease in response to refeeding (P < 0.0001). Reduced [[CIDEA]] gene expression was associated with a high body fat content (P < 0.0001) and high insulin levels (P < 0.01). No dysregulation of [[CIDEA]] expression was observed in individuals with the metabolic syndrome when compared with body mass index-matched controls. In a separate sample of VLCD-treated subjects (n = 10), uncoupling protein 1 expression was reduced during diet (P = 0.0026) and inversely associated with [[CIDEA]] expression (P = 0.0014). The findings are consistent with the concept that [[CIDEA]] plays a role in adipose tissue energy expenditure.
|mesh-terms=* Adipocytes
* Adipose Tissue
* Adult
* Aging
* Anthropometry
* Apoptosis Regulatory Proteins
* Body Composition
* Caloric Restriction
* Cross-Sectional Studies
* Female
* Gene Expression
* Humans
* Ion Channels
* Longitudinal Studies
* Male
* Metabolic Syndrome
* Metabolism
* Middle Aged
* Mitochondrial Proteins
* Obesity
* Oligonucleotide Array Sequence Analysis
* Population
* RNA
* Reverse Transcriptase Polymerase Chain Reaction
* Sex Characteristics
* Uncoupling Protein 1

|full-text-url=https://sci-hub.do/10.1210/jc.2007-1136
}}