Biochemical and Biophysical Research Communications
Regular ArticlecDNA Cloning and Expression of a Novel Adipose Specific Collagen-like Factor, apM1 (dioseost Abundant Gene Transcript 1)
Abstract
We isolated a novel adipose-specific gene, apM1, the transcript of which is the most abundant in the mRNA population from human adipose tissue. Northern blotting revealed that the human apM1 gene transcript is exclusively expressed in adipose tissue. The apM1 gene encodes a 244 amino acid open reading frame containing a putative signal sequence and G-X-Y repeats (66 amino acids) followed by a cluster of aromatic residues near the C terminus having high local similarity with collagens X and VIII and complement factor C1q. Thus, apM1 is likely to be a novel collagen-like secretory protein exclusively produced by adipose tissue.
References (0)
Cited by (1889)
Association of adiponectin and its receptor gene polymorphisms with the risk of coronary heart disease in northern Guangxi
2024, CytokineTo investigate the association of circulating adiponectin (APN) level and single nucleotide polymorphisms (rs1501299 and rs266729) of the APN gene in the coronary heart disease (CHD) population of Northern Guangxi Province.
Two hundred and sixty-three CHD patients and 235 healthy controls from our hospital from August 2018 to October 2020 were included in this study. ELISA was used to determine the serum APN concentration. PCR-RFLP and direct DNA sequencing were used to analyze the genotypes of APN gene rs1501299 G/T and rs266729 C/G single-nucleotide loci, their distribution differences between the two groups were compared and their correlation with APN concentration was analyzed.
The serum APN concentration in the CHD group was significantly lower than the control group (14.40(1.42–52.26) μg/mL vs. 29.40 (3.18–90.31) μg/mL, P < 0.001). There were statistically significant differences in the rs266729 genotype of APN single nucleotide locus between the two groups (P < 0.001). The dominant model and recessive model of rs266729 genotype showed that mutant homozygous GG genotype carriers significantly increased the risk of CHD in comparison with C allele carriers (CG + CC) (OR = 2.156, 95 %CI: 1.004–4.631, P = 0.049), and this effect was still significant after adjusting gender and age (OR = 2.695, 95 %CI 1.110–6.540, P = 0.028). In both the dominant and recessive models for rs1501299, ORs before and after adjustment for age and sex revealed no significant association with CHD, with ORs of 0.765 (95 % CI: 0.537–1.091, P = 0.139) and 0.718 (95 % CI: 0.466–1.106, P = 0.133) in the Dominant model, and ORs of 0.960 (95 % CI: 0.442–2.087, P = 0.918) and 0.613 (95 % CI: 0.239–1.570, P = 0.308) in the Recessive model, respectively. No statistically significant differences in APN concentrations across genotypes in both groups (P > 0.05), with chi-square values of 1.633 (control group) and 0.823 (CHD group) for rs1501299, and 1.354 (control group) and 0.618 (CHD group) for rs266729.
APN gene of rs266729 C/G single-nucleotide loci gene mutation can significantly increase the risk of CHD. There was no significant correlation between rs1501299 G/T single-nucleotide loci and CHD in Northern Guangxi populations.
Quantitative serum proteome analysis using tandem mass tags in dogs with epilepsy
2024, Journal of ProteomicsThis study included four groups of dogs (group A: healthy controls, group B: idiopathic epilepsy receiving antiepileptic medication (AEM), group C: idiopathic epilepsy without AEM, group D: structural epilepsy). Comparative quantitative proteomic analysis of serum samples among the groups was the main target of the study. Samples were analyzed by a quantitative Tandem-Mass-Tags approach on the Q-Exactive-Plus Hybrid Quadrupole-Orbitrap mass-spectrometer. Identification and relative quantification were performed in Proteome Discoverer. Data were analyzed using R. Gene ontology terms were analyzed based on Canis lupus familiaris database. Data are available via ProteomeXchange with identifier PXD041129. Eighty-one proteins with different relative adundance were identified in the four groups and 25 were master proteins (p < 0.05). Clusterin (CLU), and apolipoprotein A1 (APOA1) had higher abundance in the three groups of dogs (groups B, C, D) compared to controls. Amine oxidase (AOC3) was higher in abundance in group B compared to groups C and D, and lower in group A. Adiponectin (ADIPOQ) had higher abundance in groups C compared to group A. ADIPOQ and fibronectin (FN1) had higher abundance in group B compared to group C and D. Peroxidase activity assay was used to quantify HP abundance change, validating and correlating with proteomic analysis (r = 0.8796).
The proteomic analysis of serum samples from epileptic dogs indicated potential markers of epilepsy (CLU), proteins that may contribute to nerve tissue regeneration (APOA1), and contributing factors to epileptogenesis (AOC3). AEM could alter extracellular matrix proteins (FN1). Illness (epilepsy) severity could influence ADIPOQ abundance.
Positive correlation of ANGPTL8 expression in human visceral adipose tissue with body mass index
2024, Journal of the Formosan Medical AssociationAngiopoietin-like protein 8 (ANGPTL8) is an important regulator of lipid metabolism. We aimed to investigate the difference of ANGPTL8 expression in different depots of adipose tissues between individuals with and without obesity, and its correlation with various metabolic parameters.
Subcutaneous (SAT) and visceral adipose tissue (VAT) samples were collected from patients who underwent bariatric or intra-abdominal surgery. Expression levels of ANGPTL8, monoglyceride lipase (MGL), monocyte chemoattractant protein-1 (MCP-1), leptin and adiponectin (APM1) were determined using real-time quantitative polymerase chain reaction. The correlation of ANGPTL8 expression with various metabolic parameters and other gene expression levels was analyzed using Person's correlation analysis. Logistic regression was used to establish a prediction model of obesity.
Totally 330 subjects (obese: 281, non-obese: 49) were recruited. ANGPTL8 expression in VAT was significantly higher in the obesity group than in the non-obesity group (P = 0.0096). ANGPTL8 expression in VAT was positively correlated with body mass index (BMI) (r = 0.1169, P < 0.05) and was independently associated with obesity (O.R., 1.246; 95 % C.I. 1.013–21.533, P = 0.038). We also found the gene expression of ANGPTL8 in SAT and VAT was negatively correlated with APM1 expression in respective SAT and VAT.
ANGPTL8 expression levels in VAT were higher in subjects with obesity, and positively correlated with BMI. This suggests a role of ANGPTL8 in the pathophysiology of obesity and may pave the way for novel treatment target of obesity.
Intermittent fasting favorably modulates adipokines and potentially attenuates atherosclerosis
2023, Biochemical PharmacologyAdipose tissue is now recognized as an endocrine organ that secretes bioactive molecules called adipokines. These biomolecules regulate key physiological functions, including insulin sensitivity, energy metabolism, appetite regulation, endothelial function and immunity. Dysregulated secretion of adipokines is intimately associated with obesity, and translates into increased risk of obesity-related cardiovasculo-metabolic diseases. In particular, emerging evidence suggests that adipokine imbalance contributes to the pathogenesis of atherosclerosis. One of the promising diet regimens that is beneficial in the fight against obesity and cardiometabolic disorders is intermittent fasting (IF). Indeed, IF robustly suppresses inflammation, meditates weight loss and mitigates many aspects of the cardiometabolic syndrome. In this paper, we review the main adipokines and their role in atherosclerosis, which remains a major contributor to cardiovascular-associated morbidity and mortality. We further discuss how IF can be employed as an effective management modality for obesity-associated atherosclerosis. By exploring a plethora of the beneficial effects of IF, particularly on inflammatory markers, we present IF as a possible intervention to help prevent atherosclerosis.
Major depressive disorder: Biomarkers and biosensors
2023, Clinica Chimica ActaDepressive disorders belong to highly heterogeneous psychiatric diseases. Loss of in interest in previously enjoyed activities and a depressed mood are the main characteristics of major depressive disorder (MDD). Moreover, due to significant heterogeneity in clinical presentation and lack of applicable biomarkers, diagnosis and treatment remains challenging. Identification of relevant biomarkers would allow for improved disease classification and more personalized treatment strategies. Herein, we review the current state of these biomarkers and then discuss diagnostic techniques of aimed to specifically target these analytes using state of the art biosensor technology.
Obesity-mediated insulin resistance in target tissues: role of adiponectin, fetuin-A, and irisin
2023, Metabolic Syndrome: From Mechanisms to InterventionsInsulin resistance is a pathophysiologic hallmark of metabolic syndrome. This chapter highlights the role of adipokines, hepatokines, and myokines in insulin resistance. It begins with insulin resistance in target tissues, primarily adipose tissue, liver, and skeletal muscle. Since the list of secretions from these target tissues is extensive and ever-expanding, this chapter focuses on the emerging functions of three key players namely, adiponectin (an adipokine), fetuin-A (a hepato-adipokine), and irisin (an adipo-myokine), analyzing the significant role essayed by the trio in inter-organ communication deemed crucial in the pathogenesis of insulin resistance. After describing structure and biosynthesis, this chapter elaborates the signaling mechanisms of each of these in target tissues and provides detailed overview of their individual effects. It includes a discussion on inter-organ cross-talk mediated by these proteins and presents schematic representation for easy comprehension. This chapter ends with a note on their consideration as potential biomarkers of insulin resistance.
- 1
Corresponding author. Fax: +81-6-877-1922.