Редактирование: FABP1 (раздел)

==Publications==

{{medline-entry
|title=The phytochemical epigallocatechin gallate prolongs the lifespan by improving lipid metabolism, reducing inflammation and oxidative stress in high-fat diet-fed obese rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32729662
|abstract=We have recently reported that epigallocatechin gallate (EGCG) could extend lifespan in healthy rats. This study aimed to investigate the effects and mechanisms of a high dose of EGCG in extending the lifespan of obese rats. Ninety adult male Wistar rats were randomly divided into the control (NC), high-fat (HF) and EGCG groups. Serum glucose and lipids, inflammation and oxidative stress were dynamically determined from adulthood to death, and the transcriptome and proteome of the liver were also examined. The median lifespans of the NC, HF and EGCG groups were 693, 599 and 683 days, respectively, and EGCG delayed death by 84 days in obese rats. EGCG improved serum glucose and lipids and reduced inflammation and oxidative stress associated with aging in obese rats induced by a high-fat diet. EGCG also significantly decreased the levels of total free fatty acids (FFAs), SFAs and the n-6/n-3 ratio but significantly increased the n-3 FFAs related to longevity. The joint study of the transcriptome and proteome in liver found that EGCG exerted its effects mainly by regulating the suppression of hydrogen peroxide and oxygen species metabolism, suppression of oxidative stress, activation of fatty acid transport and oxidation and cholesterol metabolism. EGCG significantly increased the protein expression of [[FOXO1]], Sirt1, [[CAT]], [[FABP1]], [[GSTA2]], [[ACSL1]] and [[CPT2]] but significantly decreased NF-κB, ACC1 and [[FAS]] protein levels in the livers of rats. All the results indicate that EGCG extends lifespan by improving FFA metabolism and reducing the levels of inflammatory and oxidative stress in obese rats.

|keywords=* EGCG
* free fatty acid
* high-fat dietary
* lifespan
* proteomics
* transcriptome
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7511879
}}
{{medline-entry
|title=Expression of digestive enzyme and intestinal transporter genes during chronic heat stress in the thermally manipulated broiler chicken.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31065718
|abstract=Heat stress has a serious impact on nutrient digestion and absorption in broiler chickens. This study aimed to investigate the effects of chronic heat stress (CHS) on the mRNA expression of digestive enzymes and nutrient transporter genes in thermally manipulated (TM) broiler chickens. The evaluated genes encompassed pancreatic lipase, trypsin, amylase, maltase, and alkaline phosphatase as well as certain glucose transporter (GLUT2, SGLT1), amino acid transporter (y LAT1, CAT1), and fatty acid transporter ([[FABP1]], [[CD36]]) genes in the jejunal mucosa. Thermal manipulation was carried out at 39°C and 65% relative humidity for 18 h daily from embryonic days (ED) 10-18, while CHS was induced by raising the temperature to 35°C for 7 D throughout post-hatch days 28 to 35. After 0, 1, 3, 5, and 7 D of CHS, the pancreas and jejunal mucosa were collected from the control and TM groups to evaluate the mRNA expression by relative-quantitative real-time qRT-qPCR. Thermal manipulation significantly decreased the cloacal temperature (Tc) and the hatchling weight, and improved weight gain in broilers during post-hatch life and CHS. In addition, TM decreased the mortality rate during CHS. During CHS, the mRNA expression levels of SGLT1, GLUT2, [[FABP1]], and trypsin were significantly decreased after 1 D in control chickens, and this lower expression persisted until day 7, after which it further decreased. In contrast, in TM chickens, SGLT1, GLUT2, and [[FABP1]] expression decreased after 3, 5, and 7 D of CHS, respectively, while no significant change in trypsin expression was observed throughout the CHS period. Moreover, it was found that TM significantly modulated the mRNA expression dynamics of [[CD36]], alkaline phosphatase, y LAT1, CAT1, lipase, amylase, and maltase during CHS exposure. The findings of this study suggest that, in broiler chickens, TM has a long-lasting impact on nutrient digestion and absorption capabilities as well as Tc, mortality rates, and BW during CHS.
|mesh-terms=* Animals
* Avian Proteins
* Body Weight
* Chickens
* Cloaca
* Gastrointestinal Tract
* Gene Expression
* Hot Temperature
* Longevity
* Male
* MicroRNAs
* Random Allocation
* Reproduction
* Stress, Physiological
* Temperature
* Thermotolerance
|keywords=* broiler
* chronic heat stress
* digestive enzymes
* nutrient transporters
* thermal manipulation
|full-text-url=https://sci-hub.do/10.3382/ps/pez249
}}
{{medline-entry
|title=Manipulation of thyroid status and/or GH injection alters hepatic gene expression in the juvenile chicken.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17675858
|abstract=Both thyroid hormone (T3) and growth hormone (GH) are important regulators of somatic growth in birds and mammals. Although T3-mediated gene transcription is well known, the molecular basis of T3 interaction with GH on growth and development of birds remains unknown. In earlier studies, we discovered that exogenous GH alone increased accumulation of visceral fat in young chickens, while the combination of GH injections and dietary T3 worked synergistically to deplete body fat. In the present study, cDNA microarray and quantitative RT-PCR analyses enabled us to examine hepatic gene expression in young chickens after chronic manipulation of thyroid status and GH injection alone or in combination with T3. Thyroid status modulates expression of common and unique sets of genes involved in a wide range of molecular functions (i.e., energy metabolism, storage and transport, signal transduction, protein turnover and drug detoxification). Hepatic expression of 35 genes was altered by hypothyroidism (e.g., ADFP, [[ANGPTL3]], GSTalpha, [[CAT]], [[PPARG]], [[HMGCL]], [[GHR]], [[IGF1]], [[STAT3]], THRSPalpha), whereas hyperthyroidism affected expression of another cluster of 13 genes (e.g., [[IGFBP1]], [[KHK]], [[LDHB]], BAIA2L1, SULT1B, TRIAD3). Several genes were identified which have not been previously ascribed as T3 responsive (e.g., DEFB9, [[EPS8L2]], [[ARHGAP1]], LASS2, INHBC). Exogenous GH altered expression of 17 genes (e.g., [[CCAR1]], CYP2C45, [[GYS2]], ENOB, [[HK1]], [[FABP1]], [[SQLE]], [[SOCS2]], UPG2). The T3 GH treatment depleted the greatest amount of body fat, where 34 differentially expressed genes were unique to this group (e.g., C/EBP, [[CDC42EP1]], [[SYDE2]], [[PCK2]], PIK4CA, TH1L, [[GPT2]], BHMT). The marked reduction in body fat brought about by the T3 GH synergism could involve modulation of hormone signaling via altered activity of the Ras superfamily of molecular switches, which control diverse biological processes. In conclusion, this study provides the first global analysis of endocrine (T3 and GH) regulation of hepatic gene transcription in the chicken.
|mesh-terms=* Adipose Tissue
* Aging
* Animals
* Body Weight
* Chickens
* Gene Expression Regulation
* Growth Hormone
* Liver
* Phenotype
* RNA, Messenger
* Thyroid Gland
* Transcription, Genetic
* Triiodothyronine

|full-text-url=https://sci-hub.do/10.1159/000103178
}}