Deep spoilage is a cyclical and costly problem for the meat industry. Mianning ham is a famous dry-cured meat product in Sichuan, China. The aim of this work was to investigate the physicochemical characteristics, sources of odor, and associated microorganisms that cause spoilage of Mianning ham. High-throughput sequencing and solid-phase microextraction–gas-chromatography (SPME-GC-MS) techniques were used to characterize the physicochemical properties, microbial community structure, and volatile compounds of spoiled Mianning ham and to compare it with normal Mianning ham. The results showed that spoiled ham typically had higher moisture content, water activity (a_w), and pH, and lower salt content. The dominant bacterial phylum detected in deeply spoiled ham was Firmicutes (95.4%). The dominant bacterial genus was Clostridium_sensu_stricto_2 (92.01%), the dominant fungal phylum was Ascomycota (98.48%), and the dominant fungal genus was Aspergillus (84.27%). A total of 57 volatile flavor substances were detected in deeply spoiled ham, including 11 aldehydes, 2 ketones, 6 alcohols, 10 esters, 20 hydrocarbons, 6 acids, and 2 other compounds. Hexanal (279.607 ± 127.265 μg/kg) was the most abundant in deeply spoiled ham, followed by Butanoic acid (266.885 ± 55.439 μg/kg) and Nonanal (165.079 ± 63.923 μg/kg). Clostridium_sensu_stricto_2 promoted the formation of five main flavor compounds, Heptanal, (E)-2-Octenal, 2-Nonanone, Hexanal, and Nonanal, in deeply spoiled ham by correlation analysis of microbial and volatile flavor substances.

Satellite cells take an indispensable place in skeletal muscle regeneration, maintenance, and growth. However, only limited works have investigated effects of dietary compounds on the proliferation of porcine satellite cells (PSCs) and related mechanisms. Sulforaphane (SFN) at multiple levels was applied to PSCs. The PSCs’ viability and HDAC activity were measured with a WST-1 cell proliferation kit and Color-de-Lys^® HDAC colorimetric activity assay kit. Gene expression and epigenetics modification were tested with qRT-PCR, Western blot, bisulfite sequencing, and ChIP-qPCR. This study found that SFN enhanced PSC proliferation and altered mRNA expression levels of myogenic regulatory factors. In addition, SFN inhibited histone deacetylase (HDAC) activity, disturbed mRNA levels of HDAC family members, and elevated acetylated histone H3 and H4 abundance in PSCs. Furthermore, both mRNA and protein levels of the Smad family member 7 (SMAD7) in PSCs were upregulated after SFN treatment. Finally, it was found that SFN increased the acetylation level of histone H4 in the SMAD7 promoter, decreased the expression of microRNAs, including ssc-miR-15a, ssc-miR-15b, ssc-miR-92a, ssc-miR-17-5p, ssc-miR-20a-5p, and ssc-miR-106a, targeting SMAD7, but did not impact on the SMAD7 promoter’s methylation status in PSCs. In summary, SFN was found to boost PSC proliferation and epigenetically increase porcine SMAD7 expression, which indicates a potential application of SFN in modulation of skeletal muscle growth.

Sulforaphane (SFN) has shown diverse effects on human health and diseases. SFN was administered daily to C57BL/6J mice at doses of 1 mg/kg (SFN1) and 3 mg/kg (SFN3) for 8 weeks. Both doses of SFN accelerated body weight increment. The cross-sectional area and diameter of Longissimus dorsi (LD) muscle fibers were enlarged in SFN3 group. Triglyceride (TG) and total cholesterol (TC) levels in LD muscle were decreased in SFN groups. RNA sequencing results revealed that 2455 and 2318 differentially expressed genes (DEGs) were found in SFN1 and SFN3 groups, respectively. Based on GO enrichment analysis, 754 and 911 enriched GO terms in the SFN1 and SFN3 groups, respectively. KEGG enrichment analysis shown that one KEGG pathway was enriched in the SFN1 group, while six KEGG pathways were enriched in the SFN3 group. The expressions of nine selected DEGs validated with qRT-PCR were in line with the RNA sequencing data. Furthermore, SFN treatment influenced lipid and protein metabolism related pathways including AMPK signaling, fatty acid metabolism signaling, cholesterol metabolism signalling, PPAR signaling, peroxisome signaling, TGFβ signaling, and mTOR signaling. In summary, SFN elevated muscle fibers size and reduced TG and TC content of in LD muscle by modulating protein and lipid metabolism-related signaling pathways.

The Nanjiang Yellow Goat (NJYG), Jintang Black Goat (JTBG), and Jianzhou Da’er Goat (JZDEG) are representative local goat breeds for meat production in Sichuan Province, China. This study conducted a comprehensive evaluation of the meat quality of the longissimus dorsi muscle of three goat breeds. Variations in meat quality were observed in terms of meat pH, color, ash and fat content, water activity, and muscle fiber structure. Quantitative proteomics analysis was employed to identify biomarkers for goat meat quality, revealing hundreds of differentially expressed proteins among three goat breeds. KEGG enrichment analysis revealed enriched pathways including oxidative phosphorylation, thermogenesis, citrate cycle (TCA cycle), fatty acid degradation and metabolism, as well as valine, leucine, and isoleucine degradation. Moreover, weighted protein co-expression network analysis and protein–protein interaction analysis uncovered valuable biomarkers, including GSTM3, NDUFS, OGDH, ACO2, HADH, ACAT1, ACADS, ACAA2, HSPG2, ITGA7, PARVB, ALDH9A1, ADH5, and LOC102190016, for assessing goat meat quality. This investigation highlighted the disparities in meat quality among local goat breeds in Sichuan, China, and provided insights into underlying biological pathways and valuable biomarkers for goat meat quality.

In the efforts towards germplasm innovation of livestock and poultry, strategies to improve meat quality have faced some increasingly challenging and dynamic concerns. Intramuscular fat (IMF) content and backfat thickness are two important traits contributing to meat quality. MicroRNAs (miRNAs)—a class of endogenous noncoding RNAs maintaining cell homeostasis by inhibiting target gene expression—have been proven as critical regulators of body fat deposition, thus affecting farm animal production. Our previous in vitro and in vivo models of pigs have clarified that miR-130b overexpression can obviously suppress adipogenesis of subcutaneous preadipocytes and lower backfat thickness. However, the way miR-130b regulates proliferation and adipogenesis of primary cultured porcine intramuscular preadipocytes (PIMPA) and the underlying mechanism are still unknown. PIMPA derived from longissimus dorsi muscle were employed to examine the role of miR-130b in proliferation and adipogenesis and to further elucidate its underlying mechanism. Lipid deposition in cytoplasm was evaluated by TG quantification and ORO-staining, and EDU-staining was employed to measure cell proliferation. Adipogenic and proliferation-related gene expression were conducted by qPCR and Western blot. MiR-130b overexpression markedly stimulated proliferation of PIMPA by increasing cell cycle-related gene expression. Furthermore, overexpression of miR-130b significantly inhibited adipogenic differentiation of PIMPA, mainly by inhibiting expression of adipogenic differentiation marker genes PPAR-γ and SREBP1. In addition, we proved that miR-130b significantly inhibited expression of PPAR-γ downstream target genes and ultimately repressed adipogenesis. Ssc-miR-130b accelerated proliferation but inhibited adipogenic differentiation of PIMPA, contributing to an enhanced knowledge of the function of ssc-miR-130b in lipid deposition, and providing potential implications for enhancing pork quality.