Few studies have investigated the use of dimethylglycine sodium salt (dMG-Na) to protect against small intestinal damage, despite its prevalence in the treatment of human diseases. The present study aimed to evaluate the protective effects of dMG-Na against oxidative damage and mitochondrial dysfunction in the small intestines of mice. A total of 100 male Kunming mice were randomly assigned to five groups (n=20 per group): i) Mice gastric intubation with 0.3 ml sterile saline solution (once), then subcutaneously injected with sterile saline solution (0.5 ml) after 1 h (cON); ii) mice gastric intubation with 12 mg dMG-Na/0.3 ml of sterile saline solution once, then subcutaneously injected with sterile saline solution (0.5 ml) 1 h later (d); iii) mice gastric intubation with 0.3 ml sterile saline solution once, then subcutaneously injected with indomethacin (10 mg/kg BW) 1 h later (IN); iv) mice gastric intubation with 12 mg dMG-Na/0.3 ml sterile saline solution once, then subcutaneously injected with indomethacin (10 mg/kg BW) 1 h later (dIN); and v) mice subcutaneously injected with indomethacin (10 mg/kg BW), then gastrically intubated with 12 mg dMG-Na/0.3 ml sterile saline solution once after 1 h (INd). The present study was evaluated the effects of dMG-Na on mice intestinal damage induced by indomethacin injection. The histological morphology of the small intestine improved (P<0.05) in the dIN and INd groups, compared with the IN group. The antioxidant system was enhanced, oxidative damage was reduced, and the expression of antioxidant-associated genes was increased in the small intestine and its mitochondria in the dIN and INd groups, compared with the IN group. The above results suggested that pretreatment and treatment with dMG-Na reduced oxidative damage by enhancing antioxidant capacity, increasing the expression of antioxidant-associated genes, ameliorating mitochondrial dysfunction and suppressing apoptosis. Further study is required to determine the specific mechanism by which pretreatment and treatment with dMG-Na reduced small intestinal damage.
It is assumed that nitric oxide synthase and nitric oxide are involved in the regulation of female reproduction. This study aimed to assess the roles of nitric oxide synthase (NOS) in follicular development. The endothelial NOS (eNOS) inhibitor L-NAME, inducible NOS (iNOS) inhibitor S-Methylisothiourea (SMT) and NOS substrate L-arginine (L-Arg) were used in the NOS inhibition models in vivo. Neonatal female rats were treated with phosphate buffer saline (PBS, control), L-NAME (L-NG-Nitroarginine Methyl Ester, 40 mg/kg), SMT (S-Methylisothiourea, 10 mg/kg), L-NAME + SMT, or L-Arg (L-arginine, 50 mg/kg) via subcutaneous (SC) injection on a daily basis for 19 consecutive days, with the samples being collected on specific postnatal days (PD5, PD10, and PD19). The results indicated that the number of antral follicles, the activity of total-NOS, iNOS, neuronal NOS (nNOS), and eNOS, and the content of NO in the ovary were significantly (p < 0.05) increased in the L-Arg group at PD19, while those in L + S group were significantly (p < 0.05) decreased. Meanwhile, the ovarian expression in the L-Arg group in terms of p-AKT, p-FoxO3a, and LC3-II on PD19 were significantly (p < 0.05) upregulated, while the expressions of PTEN and cleaved Caspase-3 were (p < 0.05) downregulated as a result of NOS/NO generation, respectively. Therefore, the results suggest that NOS is possibly involved in the maturation of follicular development to puberty via the PI3K/AKT/FoxO3a pathway, through follicular autophagia and apoptosis mechanisms.
The well-documented hormonal disturbance in a general obese population is characterised by an increase in insulin secretion and a decrease in growth hormone (GH) secretion. Such hormonal disturbance promotes an increase in fat mass, which deteriorates obesity and accelerates the development of insulin resistance and type 2 diabetes. While the pathological consequence is alarming, the pharmaceutical approach attempting to correct such hormonal disturbance remains limited. By applying an emerging anti-diabetic drug, the sodium-glucose cotransporter 2 inhibitor, dapagliflozin (1 mg/kg/day for 10 weeks), to a hyperphagic obese mouse model, we observed a significant improvement in insulin and GH secretion as early as 4 weeks after the initiation of the treatment. Restoration of pathological disturbance of insulin and GH secretion reduced fat accumulation and preserved lean body mass in the obese animal model. Such phenotypic improvement followed with concurrent improvements in glucose and lipid metabolism, insulin sensitivity, as well as the expression of metabolic genes that were regulated by insulin and GH. In conclusion, 10 weeks of treatment with dapagliflozin effectively reduces hyperinsulinemia and restores pulsatile GH secretion in the hyperphagic obese mice with considerable improvement in lipid and glucose metabolism. Promising outcomes from this study may provide insights into drug intervention to correct hormonal disturbance in obesity to delay the diabetes progression.
Dietary fish oil supplementation provides n-3 long-chained polyunsaturated fatty acids for supporting fish growth and metabolism and enriching fillet with eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; c22:6n-3). Two experiments were performed as a 3 × 2 factorial arrangement of dietary treatments for 16 wk to determine effects and mechanisms of replacing 0%, 50%, and 100% fish oil with DHA-rich microalgae in combination with synthetic vs. microalgal source of astaxanthin in plant protein meal (PM)- or fishmeal (FM)- based diets for juvenile rainbow trout (Oncorhynchus mykiss). Fish (22 ± 0.26 g) were stocked at 17/tank and 3 tanks/diet. The 100% fish oil replacement impaired (P < 0.0001) growth performance, dietary protein and energy utilization, body indices, and tissue accumulation of DHA and EPA in both diet series. The impairments were associated (P < 0.05) with upregulation of hepatic gene expression related to growth (ghr1and igf1) and biosynthesis of DHA and EPA (fads6 and evol5) that was more dramatic in the FM than PM diet-fed fish, and more pronounced on tissue EPA than DHA concentrations. The source of astaxanthin exerted interaction effects with the fish oil replacement on several measures including muscle total cholesterol concentrations. In conclusion, replacing fish oil by the DHA-rich microalgae produced more negative metabolic responses than the substitution of synthetic astaxanthin by the microalgal source in juvenile rainbow trout fed 2 types of practical diets.
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