Leptin Gene Research Articles

POLYMORPHISM OF LIPID METABOLISM GENES IN TATARSTAN-TYPE COWS

POLYMORPHISM OF LIPID METABOLISM GENES IN TATARSTAN-TYPE COWS

Hippo–YAP/TAZ signalling coordinates adipose plasticity and energy balance by uncoupling leptin expression from fat mass

Adipose tissues serve as an energy reservoir and endocrine organ, yet the mechanisms that coordinate these functions remain elusive. Here, we show that the transcriptional coregulators, YAP and TAZ, uncouple fat mass from leptin levels and regulate adipocyte plasticity to maintain metabolic homeostasis. Activating YAP/TAZ signalling in adipocytes by deletion of the upstream regulators Lats1 and Lats2 results in a profound reduction in fat mass by converting mature adipocytes into delipidated progenitor-like cells, but does not cause lipodystrophy-related metabolic dysfunction, due to a paradoxical increase in circulating leptin levels. Mechanistically, we demonstrate that YAP/TAZ–TEAD signalling upregulates leptin expression by directly binding to an upstream enhancer site of the leptin gene. We further show that YAP/TAZ activity is associated with, and functionally required for, leptin regulation during fasting and refeeding. These results suggest that adipocyte Hippo–YAP/TAZ signalling constitutes a nexus for coordinating adipose tissue lipid storage capacity and systemic energy balance through the regulation of adipocyte plasticity and leptin gene transcription.

Polymorphisms of the Leptin gene in Jabres cattle

Many genes, including the leptin gene, control growth performance. Polymorphism or SNPs variant within the gene could change its expression in phenotypes. This study aimed to identify the SNP and haplotype variation of the leptin gene in Jabres cattle (n = 47 head). The SNPs variant was detected using the BioEdit version 7.0 program by sequence alignment. The HaploView program analyzed the haplotype pattern created from the SNP variants. As a result, 20 SNPs were found within the partial sequence of the leptin gene. Only 3 SNPs are located in the coding sequence (CDS) region, SNP g. 12215T>C, g.12237C>T, and g.12238G>A. For the haplotype analysis, we used only SNPs with HW p-value cutoff and minimum minor allele frequency (MAF) higher than 0.05 (Jabres = 12 SNPs). The result showed a distinctive haplotype pattern of SNPs. All the blocks of LD plot in Jabres cattle showed a high linked disequilibrium (LD) (R2 > 0.33, LOD > 2) except for the block containing SNP g.12238G>A (R2 < 0.33, LOD < 2). In conclusion, the polymorphism and haplotype pattern found in this study could be used for further association analysis to the phenotypes, and its utilization could be used as an effective marker selection tool.

Ghrelin and leptin gene expression, and adipocytes size as biomarkers in obesity rats model with Citrus amblycarpa peels extract supplementation

Ghrelin and leptin gene expression, and adipocytes size as biomarkers in obesity rats model with Citrus amblycarpa peels extract supplementation

Long-duration leptin transgene expression in dorsal vagal complex does not alter bone parameters in female Sprague Dawley rats

The hypothalamus and dorsal vagal complex (DVC) are both important for integration of signals that regulate energy balance. Increased leptin transgene expression in either the hypothalamus or DVC of female rats was shown to decrease white adipose tissue and circulating levels of leptin and adiponectin. However, in contrast to hypothalamus, leptin transgene expression in the DVC had no effect on food intake, circulating insulin, ghrelin and glucose, nor on thermogenic energy expenditure. These findings imply different roles for hypothalamus and DVC in leptin signaling. Leptin signaling is required for normal bone accrual and turnover. Leptin transgene expression in the hypothalamus normalized the skeletal phenotype of leptin-deficient ob/ob mice but had no long-duration (≥10 weeks) effects on the skeleton of leptin-replete rats. The goal of this investigation was to determine the long-duration effects of leptin transgene expression in the DVC on the skeleton of leptin-replete rats. To accomplish this goal, we analyzed bone from three-month-old female rats that were microinjected with recombinant adeno-associated virus encoding either rat leptin (rAAV-Leptin, n = 6) or green fluorescent protein (rAAV-GFP, control, n = 5) gene. Representative bones from the appendicular (femur) and axial (3rd lumbar vertebra) skeleton were evaluated following 10 weeks of treatment. Selectively increasing leptin transgene expression in the DVC had no effect on femur cortical or cancellous bone microarchitecture. Additionally, increasing leptin transgene expression had no effect on vertebral osteoblast-lined or osteoclast-lined bone perimeter or marrow adiposity. Taken together, the findings suggest that activation of leptin receptors in the DVC has minimal specific effects on the skeleton of leptin-replete female rats.

Application of Biomarkers in Obese Infertile Women: A Genetic Tool for a Personalized Treatment.

This study investigates links between CART and leptin gene expression, FSH receptor Asn680Ser polymorphism, and reproductive hormones in morbidly obese patients under 40 years old, facing infertility, and undergoing bariatric surgery. A total of 29 women were included in this study. A hormonal profile along with detection of CART and leptin gene expression was evaluated before and after bariatric surgery. Additionally, the presence or absence of Asn680Ser of the FSHR gene was studied. Following bariatric surgery, a mean reduction in BMI (16.03 kg/m2) was observed in all women. FSH levels preoperatively varied significantly among genotypes, with medians of 8.1, 9.5, and 10.3 for individuals without polymorphism, heterozygotes, and homozygotes, respectively (p = 0.0408). Post surgery, marginal differences in FSH levels were observed (5.8, 7.1, and 8.2, respectively) (p = 0.0356). E2 and LH levels exhibited no significant genotype-based differences pre and post surgery. Presurgical E2 levels were 29.6, 29.8, and 29.6, respectively (p = 0.91634), while postsurgical levels were 51.2, 47.8, and 47 (p = 0.7720). LH levels followed similar patterns. Our findings highlight bariatric surgery's positive impact on BMI reduction and its potential connection to genetic markers, hormones, and infertility. This suggests personalized treatments and offers a valuable genetic tool for better fertility outcomes in obese individuals.

The role of &lt;i&gt;LEP&lt;/i&gt; R25C polymorphism in the predisposition of cows to ketosis

In conditions of intensification of the dairy cattle industry, persistent stress of metabolic processes in the cow's body can lead to metabolic disorders and the development of ketosis. Scientists have established the genetic susceptibility of cows to ketosis. The available data allow us to consider the leptin gene (LEP) as one of the candidate genes. The purpose of the study is to carry out an associative analysis of the predisposition to ketosis of Kostroma cows of different genotypes according to the leptin gene. The research was carried out in 2022-2023 yy on clinically healthy and highly productive fresh cows of third lactation and higher of the kostroma breed (n=167) in pedigree farms of the Kostroma region. In animals in the postpartum period, the content of ketone bodies in the blood was determined by express method and the RT-PCR genotypes were determined by the R25C locus of the LEP gene. Groups of cows were formed depending on the content of ketone bodies in the blood: 1st – 0-1.2 mmol/l (healthy), 2nd – above 1.2 mmol/l (subclinical ketosis). It was found out that among the experimental cows of the Kostroma breed, the CT genotype is characterized by the highest frequency. The almost complete absence of differences in the concentration of ketone bodies in the blood between carriers of different LEP genotypes from group 1 was determined. At the same time, among the animals of the 2nd group, the highest level of ketone bodies in the blood was observed in heterozygous animals, whereas carriers of the CC and TT genotypes did not differ from each other in this indicator. Heterozygous animals classified as subclinical ketosis had the highest average ketone concentration in the blood with the highest coefficient of variation (Cv=51.6%), which indicates a pronounced influence of other genetic factors. Thus, the role of LEP R25C polymorphism in the predisposition of cows to ketosis disease has not been established in this sample of animals, but may be supplemented by the influence of other factors, these hypotheses need to be tested in a larger sample and in other breeds of cattle. These data can be used to conduct such exploratory studies, such as the research of complex genotypes of genes that cause predisposition of cattle to ketosis.

A negative feedback loop between TET2 and leptin in adipocyte regulates body weight

Ten-eleven translocation (TET) 2 is an enzyme that catalyzes DNA demethylation to regulate gene expression by oxidizing 5-methylcytosine to 5-hydroxymethylcytosine, functioning as an essential epigenetic regulator in various biological processes. However, the regulation and function of TET2 in adipocytes during obesity are poorly understood. In this study, we demonstrate that leptin, a key adipokine in mammalian energy homeostasis regulation, suppresses adipocyte TET2 levels via JAK2-STAT3 signaling. Adipocyte Tet2 deficiency protects against high-fat diet-induced weight gain by reducing leptin levels and further improving leptin sensitivity in obese male mice. By interacting with C/EBPα, adipocyte TET2 increases the hydroxymethylcytosine levels of the leptin gene promoter, thereby promoting leptin gene expression. A decrease in adipose TET2 is associated with obesity-related hyperleptinemia in humans. Inhibition of TET2 suppresses the production of leptin in mature human adipocytes. Our findings support the existence of a negative feedback loop between TET2 and leptin in adipocytes and reveal a compensatory mechanism for the body to counteract the metabolic dysfunction caused by obesity.

The effect of leptin gene polymorphisms (LEP rs7799039 and LEPR rs1137101) on febrile neutropenia

Background and aimLeptin is mainly produced in adipose tissue and released into systemic circulation. Leptin and its receptor LEPR activate the Janus kinase/signal transducers and activators of transcription signaling cascade and increase cytokine discharge. In our study, we aimed to examine the role of leptin gene (LEP) rs7799039 and LEPR rs1137101 polymorphisms on the susceptibility for febrile neutropenia (FEN) attacks and their relationship with clinical findings during the course of FEN. MethodsThis study included pediatric patients with a diagnosis of malignancy who applied to the pediatric emergency department between December 2019 and June 2022 and healthy controls. The genotypes of the LEP rs7799039 and LEPR rs1137101 genes were statistically compared between patients and healthy controls. In addition, the relationship between the genotype distribution of LEP rs7799039 and LEPR rs1137101 polymorphisms and clinical features during the course of FEN was investigated. ResultsIn the statistical analysis in terms of LEP rs7799039 and LEPR rs1137101 genotype distributions between the patient and healthy groups, there was no significant difference. Patients with the AA genotype of LEPR rs1137101 polymorphism had significantly more commonly a body mass index (BMI) value of <25, and all the patients with the AG/GG genotype had a BMI value of 25 and above. LEP rs7799039 and LEPR rs1137101 genotype distributions were not statistically significant with other clinical features. ConclusionsIt was revealed that leptin gene polymorphisms did not have a significant effect during the course of FEN.

Identification of some genetic markers as productive and reproductive traits in Ukrainian dairy cattle breeding

A Selection based on DNA markers is a breeding technique grounded in the genomic selection value of animals. The aim of the research is to study the genotypic profile of cows of different breeds in Ukrainian breeding in relation to the genes LEP, CSN3, TG5, BLG, and Pit-1 and to identify the probability of using them as markers for reproductive traits in cows. During the study, the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) method was used to analyze the genes and determine their polymorphic characteristics. The obtained data indicated that the same gene variants have varying effects in the studied breeds due to their diverse influences on the genomic background. Specifically, the homozygous state of leptin genes (LEPCC) and pituitary-specific transcription factor (PIT-1BB) was observed to impact the reproductive characteristics of cows in the evaluated breeds. Meanwhile, for the genes casein (CSN3AB), thyroglobulin (TG5CT), and beta-lactoglobulin (BLGAВ), the heterozygous state of alleles was found to influence the key reproductive traits of dairy cattle of Holstein origin. The polymorphism of the genes CSN3, βLG, TG, PIT-1, and LEP indicated the presence of genetic potential for the reproductive function of cows and can be utilized as molecular markers in selective breeding, providing significant progress in improving not only the traits of dairy cattle productivity but also reproductive function. Therefore, in the implementation of selective breeding work, it is advisable to consider genotyping for the genes CSN3, βLG, TG, PIT-1, and LEP as an additional criterion for the selection of animals to enhance both their milk and reproductive characteristics.

Classification of Congenital Leptin Deficiency.

Biallelic pathogenic leptin gene variants cause severe early-onset obesity usually associated with low or undetectable circulating leptin levels. Recently, variants have been described resulting in secreted mutant forms of the hormone leptin with either biologically inactive or antagonistic properties. We conducted a systematic literature research supplemented by unpublished data from patients at our center as well as new in vitro analyses to provide a systematic classification of congenital leptin deficiency based on the molecular and functional characteristics of the underlying leptin variants and investigated the correlation of disease subtype with severity of the clinical phenotype. A total of 28 distinct homozygous leptin variants were identified in 148 patients. The identified variants can be divided into 3 different subtypes of congenital leptin deficiency: classical hormone deficiency (21 variants in 128 patients), biologically inactive hormone (3 variants in 12 patients), and antagonistic hormone (3 variants in 7 patients). Only 1 variant (n = 1 patient) remained unclassified. Patients with biological inactive leptin have a higher percentage of 95th body mass index percentile compared to patients with classical hormone deficiency. While patients with both classical hormone deficiency and biological inactive hormone can be treated with the same starting dose of metreleptin, patients with antagonistic hormone need a variant-tailored treatment approach to overcome the antagonistic properties of the variant leptin. Categorization of leptin variants based on molecular and functional characteristics helps to determine the most adequate approach to treatment of patients with congenital leptin deficiency.

Association of Polymorphism in Leptin Gene with Semen Quality Parameters in Egyptian Buffaloes Bulls

Association of Polymorphism in Leptin Gene with Semen Quality Parameters in Egyptian Buffaloes Bulls

AMP-activated protein kinase activation suppresses leptin expression independently of adipogenesis in primary murine adipocytes.

Adipogenesis, defined as the development of mature adipocytes from stem cell precursors, is vital for the expansion, turnover and health of adipose tissue. Loss of adipogenic potential in adipose stem cells, or impairment of adipogenesis is now recognised as an underlying cause of adipose tissue dysfunction and is associated with metabolic disease. In this study, we sought to determine the role of AMP-activated protein kinase (AMPK), an evolutionarily conserved master regulator of energy homeostasis, in adipogenesis. Primary murine adipose-derived stem cells were treated with a small molecule AMPK activator (BI-9774) during key phases of adipogenesis, to determine the effect of AMPK activation on adipocyte commitment, maturation and function. To determine the contribution of the repression of lipogenesis by AMPK in these processes, we compared the effect of pharmacological inhibition of acetyl-CoA carboxylase (ACC). We show that AMPK activation inhibits adipogenesis in a time- and concentration-dependent manner. Transient AMPK activation during adipogenic commitment leads to a significant, ACC-independent, repression of adipogenic transcription factor expression. Furthermore, we identify a striking, previously unexplored inhibition of leptin gene expression in response to both short-term and chronic AMPK activation irrespective of adipogenesis. These findings reveal that in addition to its effect on adipogenesis, AMPK activation switches off leptin gene expression in primary mouse adipocytes independently of adipogenesis. Our results identify leptin expression as a novel target of AMPK through mechanisms yet to be identified.

Personalization of treatment based on obesity phenotypes

Introduction:&#x0D; Obesity is a significant clinical problem worldwide. The disease exhibits remarkable heterogeneity, leading to diverse pathogenesis among individuals. Despite a growing selection of weight-reducing medications and increased awareness of the importance of a healthy lifestyle, the effectiveness of obesity therapy often remains insufficient. This raises the question of whether tailoring obesity pharmacotherapy to specific phenotypes and individual patient characteristics results in improved treatment outcomes.&#x0D; Objective:&#x0D; To review literature on the effectiveness of obesity treatment based on the personalization of pharmacotherapy according to its underlying causes.&#x0D; Current Knowledge:&#x0D; Currently, the early outcome of weight loss is closely linked to the long-term effectiveness of obesity pharmacotherapy. However, due to the diversity of obesity pathogenesis, it is not helpful in selecting therapy at the initiation of treatment. Specific characteristics are sought to indicate the appropriate drug during therapy planning.&#x0D; In a U.S. study (Acosta et al., 2021) results showed that phenotype-guided obesity pharmacotherapy resulted in clinically more significant absolute weight loss than in the non-phenotyped group.&#x0D; Other studies demonstrated that for very rare types of obesity dependent on specific genetic mutations, targeted treatment addressing these defects yielded the best therapeutic outcomes (recombinant human leptin therapy for patients with leptin gene mutation – Farooqi et al., 2002; setmelanotide therapy for individuals with proopiomelanocortin deficiency – Clément et al., 2020).&#x0D; The impact of specific gene variants on therapeutic response should also be considered, leading to variability in treatment effects for different patients using the same drug.&#x0D; Conclusion:&#x0D; The concept of basing therapy on obesity phenotypes may currently serve as a guide for treatment selection, although it still requires confirmation in randomized clinical trials.&#x0D;

Prospective Study on the Correlation between CART and Leptin Gene Expression, Obesity, and Reproductive Hormones in Individuals Undergoing Bariatric Surgery.

Obesity, a global health concern affecting 650 million individuals of all ages worldwide, prompts health complications, including fertility issues. This research investigates the impact of bariatric surgery on morbidly obese females under 40, examining the relationship between CART and leptin gene expressions and reproductive hormones. Post-surgery, a significant reduction in BMI (16.03 kg/m2, n = 29) was observed, accompanied by notable hormonal changes. FSH levels showed a mean difference of 3.18 ± 1.19 pre- and post-surgery (p < 0.001), LH levels exhibited a mean difference of 2.62 ± 1.1 (p < 0.001), E2 levels demonstrated a mean difference of 18.62 ± 5.02 (p < 0.001), and AMH levels showed a mean difference of 3.18 ± 1.19 (p < 0.001). High CART and leptin expressions before treatment correlated with lower expressions after treatment. These findings, rooted in statistically significant correlations (CART: rs = 0.51, p = 0.005; leptin: rs = 0.75, p < 0.001), shed light on potential molecular pathways connecting gene expressions with reproductive hormones post-bariatric surgery. Our study uniquely investigates the interplay between genetic markers, infertility, and bariatric surgery in women. It stands out by providing distinctive insights into the development of personalized treatment strategies for obesity-related infertility, contributing to a deeper understanding of this complex medical issue.

Adiponectin Resistance in Obesity: Adiponectin Leptin/Insulin Interaction.

The adiponectin (APN) levels in obesity are negatively correlated with chronic subclinical inflammation markers. The hypertrophic adipocytes cause obesity-linked insulin resistance and metabolic syndrome. Furthermore, macrophage polarization is a key determinant regulating adiponectin receptor (AdipoR1/R2) expression and differential adiponectin-mediated macrophage inflammatory responses in obese individuals. In addition to decrease in adiponectin concentrations, the decline in AdipoR1/R2 messenger ribonucleic acid (mRNA) expression leads to a decrement in adiponectin binding to cell membrane, and this turns into attenuation in the adiponectin effects. This is defined as APN resistance, and it is linked with insulin resistance in high-fat diet-fed subjects. The insulin-resistant group has a significantly higher leptin-to-APN ratio. The leptin-to-APN ratio is more than twofold higher in obese individuals. An increase in expression of AdipoRs restores insulin sensitivity and β-oxidation of fatty acids via triggering intracellular signal cascades. The ratio of high molecular weight to total APN is defined as the APN sensitivity index (ASI). This index is correlated to insulin sensitivity. Homeostasis model of assessment (HOMA)-APN and HOMA-estimated insulin resistance (HOMA-IR) are the most suitable methods to estimate the metabolic risk in metabolic syndrome. While morbidly obese patients display a significantly higher plasma leptin and soluble (s)E-selectin concentrations, leptin-to-APN ratio, there is a significant negative correlation between leptin-to-APN ratio and sP-selectin in obese patients. When comparing the metabolic dysregulated obese group with the metabolically healthy obese group, postprandial triglyceride clearance, insulin resistance, and leptin resistance are significantly delayed following the oral fat tolerance test in the first group. A neuropeptide, Spexin (SPX), is positively correlated with the quantitative insulin sensitivity check index (QUICKI) and APN. APN resistance together with insulin resistance forms a vicious cycle. Despite normal or high APN levels, an impaired post-receptor signaling due to adaptor protein-containing pleckstrin homology domain, phosphotyrosine-binding domain, and leucine zipper motif 1 (APPL1)/APPL2 may alter APN efficiency and activity. However, APPL2 blocks adiponectin signaling through AdipoR1 and AdipoR2 because of the competitive inhibition of APPL1. APPL1, the intracellular binding partner of AdipoRs, is also an important mediator of adiponectin-dependent insulin sensitization. The elevated adiponectin levels with adiponectin resistance are compensatory responses in the condition of an unusual discordance between insulin resistance and APN unresponsiveness. Hypothalamic recombinant adeno-associated virus (rAAV)-leptin (Lep) gene therapy reduces serum APN levels, and it is a more efficient strategy for long-term weight maintenance.

Comparison of genetic diversity of LEP gene between Indonesia domestic goats: Etawa Cross and Senduro Goats

Abstract. Amrullah MF, Utomo B, Utama S, Lestari TD, Suprayogi TW, Restiadi TI, Belgania RH, Pakpahan S, Khairullah AR, Kurniawan SC, Silaen OSM, Hasib A. 2023. Comparison of genetic diversity of LEP gene between Indonesia domestic goats: Etawa Cross and Senduro Goats. Biodiversitas 24: 6567-6573. The leptin (LEP) gene is a gene that functions to produce the hormone leptin secreted by fat tissue that can increase livestock productivity. This study aimed to identify the profile of the LEP gene between Etawah Cross goats and Senduro goats. Gene profiling includes single nucleotide polymorphisms (SNPs) and phylogeny tree reconstruction. Furthermore, 10 whole blood samples from 5 Etawah Cross goats and 5 Senduro goats were collected from goat farms in Lumajang District, Lumajang Regency, Indonesia. The Research procedure involved collecting blood samples, extracting DNA, amplification using the polymerase chain reaction (PCR) method using specific primers, and nucleotide sequencing method. The edited DNA sequences were aligned with some DNA sequences (n=32) of the Capra hircus group published in Genbank. The results of this study obtained the alignment of the LEP gene sequences of Etawah Cross goats and Senduro goats, including T723A, G729A, G758A, A763T, G774C, T1100C, and G1454A. Based on the LEP gene phylogeny tree, Etawah Cross goats and Senduro goats belong to the same clade and have a close kinship with the Bligon goats. The profile of the LEP gene between Etawah Cross goats and Senduro goats varies so that further studies can be carried out to look for the relationship between SNPs and the productivity traits of the LEP gene.

Oleoylethanolamide protects mesenchymal stem/stromal cells (MSCs) from oxidative stress and reduces adipogenic related genes expression in adipose-derived MSCs undergoing adipocyte differentiation.

Human mesenchymal stem/stromal cells (hMSCs) are known for their pronounced therapeutic potential; however, they are still applied in limited clinical cases for several reasons. ROS-mediated oxidative stress is among the chief causes of post-transplantation apoptosis and death of hMSCs. It has been reported that a strategy to protect hMSCs against ROS is to pretreat them with antioxidants. Oleoylethanolamide (OEA) is a monounsaturated fatty acid derived from oleic acid and it has many protective properties, including anti-obesity, anti-inflammatory, and antioxidant effects. OEA is also used as a weight loss supplement; due to its high affinity for the PPAR-α receptor, OEA increases the fat metabolism rate. This study hence assessed the effects of OEA pretreatment on the in vitro survival rate and resistance of hMSCs under oxidative stress as well as the cellular and molecular events in the biology of stem/stromal cells affected by oxidative stress and free radicals. Considering the role of MSCs in adipogenesis and obesity, the expression of the main genes involved in adipogenesis was also addressed in this study. Results revealed that OEA increases the in vitro proliferation of MSCs and inhibits cell apoptosis by reducing the induction of oxidative stress. The results also indicated that OEA exerts its antioxidant properties by both activating the Nrf2/NQO-1/HO-1 signaling pathway and directly combating free radicals. Moreover, OEA can reduce adipogenesis through reducing the expression of PPARγ, leptin and CEBPA genes in hMSCs undergoing adipocyte differentiation. Thus, OEA protects hMSCs from oxidative stress and reduces adipogenic related genes expression and can be regarded as a therapeutic agent for this purpose.

Correlation analysis between polymorphism of leptin and IGFI genes and body measurements in Barki and Farafra sheep

BackgroundGrowth performance, which can be evaluated using various body measurements, is crucial for providing red meat for human consumption. This study aims to improve the growth performance of sheep by identifying the different genotypes of leptin and IGFI genes associated with higher body measurements.MethodsIn this study, we collected blood samples from Barki (n = 30) and Farafra (n = 30) sheep, and measured their body height, width, length, and weight, and tail width and length to assess their growth performance. We used single strand conformation polymorphism polymerase chain reaction (SSCP-PCR) and sequencing analysis to identify single nucleotide polymorphisms (SNPs) and different genotypes of the leptin and insulin-like growth factor receptor (IGFI) genes associated with sheep body measurements.ResultsThe leptin gene (209 bp) and IGFR gene (345 bp) were found to have three (TT, TG, and GG) and (TT, TC, and CC) genotypes, respectively, by SSCP-PCR. Sequence analysis revealed a SNP in the leptin gene (200G > T) with two alleles (G allele: OR058867 and T allele: OR058868). This SNP resulted in the substitution of the amino acid valine with leucine, which increased the width, length, and weight of the body and tail width in the heterozygous form (TG). The IGFI gene had three SNPs: 305 G > T in TT genotype (OR260670), 184C > T, 265T > C, and 305G > T in TC genotype (OR260669), and 265T > C in CC genotype (OR260671). The TC genotype of the IGFR gene was correlated with higher values of body measurements. Barki sheep were found to have the highest values for body weight, width, length, and tail width compared to Farafra sheep.ConclusionWe recommend the use of entire Barki sheep in inbreeding programs to improve growth performance in Egyptian sheep.

Identification of genes related to growth from transcriptome profiles of the muscle and liver of Chinese longsnout catfish (Leiocassis longirostris)

The Chinese longsnout catfish (Leiocassis longirostris) is a commercially important freshwater fish species in China. To understand the molecular mechanisms underlying its growth, we performed a comparative transcriptomic analysis of muscle and liver tissues of fast- and slow-growing L. longirostris. A total of 580 and 511 differentially expressed genes (DEGs) were obtained in the muscle and liver tissues, respectively. We selected 10 DEGs each from muscle and liver tissues by qRT-PCR to verify the reliability of RNA-seq, and it was found that the expression patterns of these genes were consistent with RNA-seq analysis results. According to the differential expression and functional enrichment analysis of genes, we found differences in the expression of several growth-related genes between fast- and slow-growing individuals. These genes may contribute to the differences in the growth of L. longirostris by influencing muscle growth and the metabolism of substances and energy. In particular, the pk and fabp genes were highly expressed in fast-growing individuals, while the cart, leptin, pepck, murf1, trim32, and pparα genes exhibited higher levels in slow-growing individuals. It was speculated that genes related to feeding behavior might be the key genes in regulating the growth of L. longirostris, while glycolytic/gluconeogenic metabolic pathway, lipid metabolism, and ubiquitin-proteasome pathway might be the main pathways involved in regulating body weight of L. longirostris. This study could enrich the available gene resources and provide a valuable basis for further studies on the regulatory mechanisms of growth in L. longirostris.