Tricaprylin, a medium-chain triglyceride, aggravates high-fat diet-induced fat deposition but improves intestinal health.

Medium-chain triglycerides (MCTs) are absorbed and metabolized more rapidly than long-chain triglycerides (LCTs) and therefore are considered to have obesity-prevention potential in foods. The effect of adding tricaprylin, an MCT, to food on fat deposition and intestinal health is uncharted. In this study, mice were randomly divided into four groups and fed a normal diet (ND), ND with tricaprylin, a high-fat diet (HFD), or HFD with tricaprylin. Supplementation of 2% tricaprylin in HFD significantly increased the body weight, fat mass, liver weight, adipocyte size in adipose tissue and liver, and upregulated genes related to fat deposition. Metabolomic analysis of serum and adipose tissue revealed that tricaprylin significantly increased the contents of metabolites related to lipid metabolism, triglyceride storage, and fat deposition related signaling pathways. In vitro experiments and molecular docking analysis suggest that octanoic acid, a primary decomposition product of tricaprylin, may promote adipogenic differentiation of preadipocytes by acting as a PPARγ ligand to activate the expression of lipogenesis-related genes. Although supplementation with 2% tricaprylin in HFD cannot reduce fat deposition, it has a beneficial effect on intestinal health. Tricaprylin improved intestinal morphology, digestive enzyme activity, short-chain fatty acid concentration, and intestinal barrier function-related protein expression, while reducing inflammatory factor levels and the abundance of harmful intestinal microorganisms.

Melatonin promotes gut anti-oxidative status in perinatal rat by remodeling the gut microbiome.

Gut health is important for nutrition absorption, reproduction, and lactation in perinatal and early weaned mammals. Although melatonin functions in maintaining circadian rhythms and preventing obesity, neurodegenerative diseases, and viral infections, its impact on the gut microbiome and its function in mediating gut health through gut microbiota remain largely unexplored. In the present study, the microbiome of rats was monitoring after fecal microbiota transplantation (FMT) and foster care (FC). The results showed that FMT and FC increased intestinal villus height/crypt depth in perinatal rats. Mechanistically, the melatonin-mediated remodeling of gut microbiota inhibited oxidative stress, which led to attenuation of autophagy and inflammation. In addition, FMT and FC encouraged the growth of more beneficial intestinal bacteria, such as Allobaculum, Bifidobacterium, and Faecalibaculum, which produce more short-chain fatty acids to strengthen intestinal anti-oxidation. These findings suggest that melatonin-treated gut microbiota increase the production of SCFAs, which improve gut health by reducing oxidative stress, autophagy and inflammation. The transfer of melatonin-treated gut microbiota may be a new and effective method by which to ameliorate gut health in perinatal and weaned mammals.

miR-503 targets MafK to inhibit subcutaneous preadipocyte adipogenesis causing a decrease of backfat thickness in Guanzhong Black pigs.

Reducing backfat thickness (BFT), determined by subcutaneous fat deposition, is vital in Chinese developed pig breeds. The level of miR-503 in the backfat of Guanzhong Black pigs was found to be lower than that in Large White pigs, implying that miR-503 may be related to BFT. However, the effect and mechanism of miR-503 on adipogenic differentiation in subcutaneous preadipocytes remain unknown. Compared with Large White pigs, the BFT and body fat content of Guanzhong Black pigs were greater, but the level of miR-503 was lower in subcutaneous adipose tissue (SAT) at 180 days of age. Furthermore, miR-503 promoted preadipocyte proliferation by increasing the proportion of S-phase and EdU-positive cells. However, miR-503 inhibited preadipocyte differentiation by downregulating adipogenic gene expression. Mechanistically, miR-503 directly targeted musculoaponeurotic fibrosarcoma oncogene homolog K (MafK) in both proliferating and differentiating preadipocytes to repress adipogenesis. Our findings provide a novel miRNA biomarker for reducing pig BFT levels to improve carcass quality.

COPS3 AS lncRNA enhances myogenic differentiation and maintains fast-type myotube phenotype.

Long non-coding RNAs (lncRNAs) play essential roles in myogenesis. Here, we identified a novel long non-coding RNA, named COPS3 AS lncRNA (COP9 signalosome complex subunit 3 antisense lncRNA), which was transcribed from the mouse COPS3 gene antisense strand and highly expressed in glycolytic muscle fibers. Functionally, COPS3 AS lncRNA knockdown inhibited myogenic differentiation in myoblasts, whereas its overexpression promoted the process. Moreover, COPS3 AS lncRNA maintained the fast-twitch myotubes phenotype. Mechanistically, although COPS3 AS lncRNA did not form AS lncRNA/mRNA dimer with COPS3 mRNA, it as a competing endogenous RNA (ceRNA) to sponge miR-762, promoted myogenic differentiation and Fast-MyHC expression by modulating miR-762 target gene myogenic differentiation 1 (MyoD1). Taken together, COPS3 AS lncRNA is a key candidate regulator of myogenesis and fast-MyHC myotubes specification by miR-762/MyoD signalling axis.

Dietary Supplementation With Acer truncatum Oil Promotes Remyelination in a Mouse Model of Multiple Sclerosis.

Background: Multiple sclerosis is a chronic demyelinating disease of uncertain etiology. Traditional treatment methods produce more adverse effects. Epidemiological and clinical treatment findings showed that unknown environmental factors contribute to the etiology of MS and that diet is a commonly assumed factor. Despite the huge interest in diet expressed by people with MS and the potential role diet plays in MS, very little data is available on the role of diet in MS pathogenesis and MS course, in particular, studies on fats and MS. The oil of Acer truncatum is potential as a resource to be exploited in the treatment of some neurodegenerative diseases. Objective: Here, we investigated the underlying influences of Acer truncatum oil on the stimulation of remyelination in a cuprizone mouse model of demyelination. Methods: Cuprizone (0.2% in chow) was used to establish a mouse model of demyelination. Acer truncatum oil was administrated to mice during remyelination. Following techniques were used: behavioral test, histochemistry, fluorescent immunohistochemistry, transmission electron microscope. Results: Mice exposed to cuprizone for 6 weeks showed schizophrenia-like behavioral changes, the increased exploration of the center in the open field test (OFT), increased entries into the open arms of the elevated plus-maze, as well as demyelination in the corpus callosum. After cuprizone withdrawal, the diet therapy was initiated with supplementation of Acer truncatum oil for 2 weeks. As expected, myelin repair was greatly enhanced in the demyelinated regions with increased mature oligodendrocytes (CC1) and myelin basic protein (MBP). More importantly, the supplementation with Acer truncatum oil in the diet reduced the schizophrenia-like behavior in the open field test (OFT) and the elevated plus-maze compared to the cuprizone recovery group. The results revealed that the diet supplementation with Acer truncatum oil improved behavioral abnormalities, oligodendrocyte maturation, and remyelination in the cuprizone model during recovery. Conclusion: Diet supplementation with Acer truncatum oil attenuates demyelination induced by cuprizone, indicating that Acer truncatum oil is a novel therapeutic diet in demyelinating diseases.

Prolonged maternal separation alters neurogenesis and synaptogenesis in postnatal dentate gyrus of mice.

OBJECTIVES: As a common model for adverse early experience and depression, maternal separation (MS) is always used to investigate the psychological disease. Despite extensive and strong evidence verified the depression-like state induced by MS, little is known about the specific mechanism of MS. Therefore, the present study aimed to investigate the neurobiology mechanism of the MS-induced depression-like state. METHODS: To verify the depression-like behaviors of offspring induced by MS, a series of behavioral tests were performed. Then, in vivo electroporation and three-dimensional reconstruction, combining with immunohistochemistry and BrdU labeling, were mainly used to explore the neurogenesis and synaptogenesis in postnatal dentate gyrus. RESULTS: Prolonged MS indeed induced the depression-like behaviors of offspring in adulthood. Surprisingly, learning and memory were enhanced by prolonged MS. Further investigation indicated that prolonged MS inhibited the proliferation of neural stem cells, impaired the survival, and altered the fate decision of newborn cells, whereas the total length and terminal tips of dendrite, and the spine density, especially thin spine, were significantly increased in prolonged MS mice. CONCLUSIONS: Our results elucidated that prolonged MS induced the depression-like state by impairing postnatal neurogenesis of dentate gyrus. Importantly, our results emphasized that prolonged MS increased the spine density, especially thin spine, by increasing the total length and number of terminal tips of dendrite, thereby enhancing learning and memory.

Prenatal Exposure to Gossypol Impairs Corticogenesis of Mouse.

Gossypol is a yellow polyphenolic compounds extracted from roots, stems and seeds of cotton plants. Excessive intake of gossypol induces severe pathological signs of toxicity in livestock and wildlife. Currently, gossypol has received widespread attention for its toxic effects on the reproductive system. However, reports of the effects of gossypol during corticogenesis and the development of the mouse cerebral cortex are unavailable. In the present study, gossypol was orally administrated at a dose of 0, 20, and 50 mg/kg body weight/day to pregnant mice from embryonic day 6.5 to the time of sample collection. We used in utero electroporation and immunofluorescence to demonstrate that gossypol impaired cortical neuronal migration. Furthermore, labeling with 5-bromo-2-deoxyuridine and western blot analysis revealed that gossypol disturbed the balance between proliferation and differentiation of neural progenitors, inhibited neural progenitor cell proliferation, neuronal differentiation, and maturation. Additionally, cortical progenitor apoptotic cell death increased in the developing gossypol-treated cortex, which was associated with NF-κB and MAPK pathways. In conclusion, our findings indicate that gossypol exposure disrupted neurogenesis in the developing neocortex, suggesting the potentially harmful impact of gossypol on the cerebral cortex development of humans and livestock.

[Process in menstrual blood-derived mesenchymal stem cells for treatment of central nervous system diseases].

Stem cell research has become a frontier in the field of life sciences, and provides an ideal model for exploring developmental biology problems such as embryogenesis, histiocytosis, and gene expression regulation, as well as opens up new doors for clinical tissue defective and inheritance diseases. Among them, menstrual blood-derived stem cells (MenSCs) are characterized by wide source, multi-directional differentiation potential, low immune rejection characteristics. Thus, MenSCs can achieve individual treatment and have the most advantage of the clinical application. The central nervous system, including brain and spinal cord, is susceptible to injury. And lethality and morbidity of them tops the list of all types of trauma. Compared to peripheral nervous system, recovery of central nervous system after damage remains extremely hard. However, the treatment of stem cells, especially MenSCs, is expected to solve this problem. Therefore, biological characteristics of MenSCs and their treatment in the respect of central nervous system diseases have been reviewed at home and abroad in recent years, so as to provide reference for the treatment of central nervous system diseases.