Pantothenic Acid Alleviates Fat Deposition and Inflammation by Suppressing the JNK/P38 MAPK Signaling Pathway.

Excessive fat deposition leads to obesity and cardiovascular diseases with abnormal metabolism. Pantothenic acid (PA) is a major B vitamin required for energy metabolism. However, the effect of PA on lipid metabolism and obesity has not been explored. We investigated the effects and molecular mechanism of PA on fat accumulation as well as the influence of adipogenic marker genes in both adult male mice and primary adipocytes. First, we demonstrated that PA attenuates weight gain in mice fed high-fat diet (HFD). Besides, PA supplementation substantially improved glucose tolerance and lipid metabolic disorder in obese mice. Furthermore, PA significantly inhibited white adipose tissue (WAT) deposition as well as fat droplets visualized by magnification in both chow and HFD group. More importantly, PA obviously suppressed the mRNA levels of CD36, IL-6, and TNF-α to alleviate inflammation and reduced the levels of PPARγ, aP2, and C/EBPα genes that are related to lipid metabolism in inguinal white adipose tissue (ing-WAT) and epididymal white adipose tissue (ei-WAT). In vitro, PA supplementation showed a lower lipid droplet aggregation as well as reduced expression levels of adipogentic genes. Finally, we identified that PA inhibits the phosphorylation levels of p38 and JNK in murine primary adipocytes. Collectively, our data demonstrated for the first time that PA attenuates lipid metabolic disorder as well as fat deposition by JNK/p38 MAPK signaling pathway.

Reassessment of adipocyte technology for cellular agriculture of alternative fat.

Alternative proteins, such as cultivated meat, have recently attracted significant attention as novel and sustainable food. Fat tissue/cell is an important component of meat that makes organoleptic and nutritional contributions. Although adipocyte biology is relatively well investigated, there is limited focus on the specific techniques and strategies to produce cultivated fat from agricultural animals. In the assumed standard workflow, stem/progenitor cell lines are derived from tissues of animals, cultured for expansion, and differentiated into mature adipocytes. Here, we compile information from literature related to cell isolation, growth, differentiation, and analysis from bovine, porcine, chicken, other livestock, and seafood species. A diverse range of tissue sources, cell isolation methods, cell types, growth media, differentiation cocktails, and analytical methods for measuring adipogenic levels were used across species. Based on our analysis, we identify opportunities and challenges in advancing new technology era toward producing "alternative fat" that is suitable for human consumption.

C/EBPb converts bovine fibroblasts to adipocytes without hormone cocktail induction

BACKGROUND: Adipogenesis and fibrogenesis can be considered as a competitive process in muscle, which may affect the intramuscular fat deposition. The CCAAT/enhancer-binding protein beta (C/EBPb) plays an important role in adipogenesis, which is well-characterized in mice, but little known in bovine so far. RESULTS: In this study, real-time qPCR revealed that the level of C/EBPb was increased during the developmental stages of bovine and adipogenesis process of preadipocytes. Overexpression of C/EBPb promoted bovine fibroblast proliferation through mitotic clonal expansion (MCE), a necessary process for initiating adipogenesis, by significantly downregulating levels of p21 and p27 (p < 0.01). Also, the PPARc expression was inhibited during the MCE stage (p < 0.01). 31.28% of transfected fibroblasts adopted lipid-laden adipocyte morphology after 8 d. Real-time qPCR showed that C/EBPb activated the transcription of early stage adipogenesis markers C/EBPa and PPARc. Expression of ACCa, FASN, FABP4 and LPL was also significantly upregulated, while the expression of LEPR was weakened. CONCLUSIONS: It was concluded C/EBPb can convert bovine fibroblasts into adipocytes without hormone induction by initiating the MCE process and promoting adipogenic genes expression, which may provide new insights into the potential functions of C/EBPb in regulating intramuscular fat deposition in beef cattle.

EFFECT OF HYPEROSIDE ON THE INHIBITION OF ADIPOGENESIS IN 3T3-L1 ADIPOCYTES.

CONTEXT: The inhibition of adipocyte differentiation has a significant role on the prevention of obesity and obesity-associated complications. OBJECTIVE: In this study, we aimed to detect whether hyperoside is able to inhibit the conversion of pre-adiposits into mature adiposits. DESIGN AND METHODS: 3T3-L1 pre-adipocytes were stimulated so as to differentiate into mature adipocytes. Hyperoside in non-cytotoxic concentrations (1, 2, 5, and 10 µM) were separately applied to differentiated 3T3-L1 cells. Oil red O staining was performed and triacylglycerol contents were measured. Furthermore, gene and protein expressions of transcription factors, adipogenic genes and adipokines were examined in order to investigate the effect of hyperoside on adipocyte differentiation. RESULTS: Hyperoside in high concentrations significantly suppressed the adipogenic process by inhibiting the expression of transcription factors and adipogenic genes and reducing lipid accumulation in adipocytes (p<0.05). Low doses of hyperoside are able to inhibit adipogenesis, but higher doses are needed to reduce fat accumulation in mature adipocytes. In the case of maturing preadipocytes, 5 µM of hyperoside exerts its antiadipogenic effect at the early stages of adipogenesis, whereas 10 µM of hyperoside acts at the later stages (p<0.05). CONCLUSION: These results suggest that hyperoside has a beneficial effect on the prevention and treatment of obesity.