Purification, characterization and antibacterial spectrum of a compound produced by Bacillus cereus MTCC 10072.

Awareness of the consumer has increased the demand of safe and chemical-free foods, and consequently it has increased the demand of antibacterial bioactive compounds. In the present study, antibacterial compound produced by a local bacterial isolate NSD MTCC 10072, showing antagonistic activity against six human pathogens, was isolated, partially purified and characterized. Maximum production of antibacterial compound was observed between 51 and 60 h after seeding. The antibacterial activity of the compound was found to be thermostable up to 80 °C for 60 min and its efficacy was very good between pH 4 and 12. Minimum inhibitory concentration (25.84 µg/µl) of the antibacterial compound was observed against Streptococcus aureus NICM 2901. GC-MS analysis of the bacterium secreted chemical compound (C11H18N2O2) was used to identify the antimicrobial compound as Pyrrolo(1,2-a) pyrazine-1,4-dione, hexahydro-3-(2-methylpropyl). In Silico studies showed that the antimicrobial compound is non-toxic, non-irritating and followed Lipinski-type properties which suggested that the compound could be used as potential drug against different human pathogens.

Dietary n-3 and n-6 polyunsaturated fatty acids differentially modulate the adiponectin and leptinmediated major signaling pathways in visceral and subcutaneous white adipose tissue in high fat diet induced obesity in Wistar rats.

Obesity is a chronic metabolic disease that involves excessive accumulation of fat in white adipose tissue (WAT). Apart from storing excess fats, WAT also serves as an important endocrine organ secreting adipocytokines such as adiponectin and leptin. Adiponectin and leptin bind to their transmembrane receptors adiponectin receptor 1 (AdipoR1)/adiponectin receptor 2 (AdipoR2) and Ob-R, respectively, and mediate their effect on metabolism by regulating multiple downstream targets. Dietary fat is considered the main culprit behind obesity development. Numerous preclinical studies have highlighted role of essential polyunsaturated fatty acids (PUFAs), particularly n-3 PUFAs, in prevention of obesity. Despite emerging data, there still is no clear understanding of the mechanism of action of n-3 PUFAs and n-6 PUFAs on adipose tissue function in two functionally and anatomically different depots of WAT: visceral and subcutaneous. We designed this study using a high fat diet (HFD) fed rodent model of obesity to test our hypothesis that n-3 and n-6 PUFAs possibly differentially modulate adipokine secretion and downstream metabolic pathways such as peroxisome proliferator-activated receptor-γ (PPAR-γ), protein kinase B (AKT)-forkhead box O1 (FOXO1), and Janus kinase-signal transducer and activator of transcription in obesity. The results of the current study showed that n-3 PUFAs upregulate the expression of AdipoR1/R2 and ameliorate the effects of HFD by modulating adipogenesis via PPAR-γ and by improving glucose tolerance and lipid metabolism via AKT-FOXO1 axis in fish oil fed rats. However, n-6 PUFAs did not show any remarkable change compared with HFD fed animals. Our study highlights that n-3 PUFAs modulate expression of various targets in adiponectin and leptin signaling cascade, bringing about an overall reduction in obesity and improvement in adipose tissue function in HFD induced obesity.

Pine nut oil supplementation alleviates the obesogenic effects in high-fat diet induced obese rats: A comparative study between epididymal and retroperitoneal adipose tissue.

Pine nut oil (PNO) is a rich source of polyunsaturated fatty acids. It is obtained from species such as Pinus siberica, Pinus gerardinia, Pinus koraiensis, and so on. A few studies have shown its protective effect against obesity by regulating lipid metabolism and suppressing appetite. However, its effect on the release of adipokines and obesity-associated signaling pathways is yet to be investigated. We hypothesized that PNO might exert its antiobesogenic effects by modulating adiponectin/leptin-mediated cell signaling pathways. Therefore, the present study was designed to investigate the mechanism of action of 10% PNO substitution on the high-fat diet-induced obesity in male Wistar rats. PNO incorporation in the diet significantly decreased the body weight, body mass index, Lee index, liver weight, blood glucose levels, and adipose tissue size. It also reduced the levels of proinflammatory cytokines (interleukin-6 and tumor necrosis factor-α) and triglycerides and increased levels of high-density lipoprotein cholesterol in serum significantly. It was observed that incorporation of PNO led to a significant increase in ADIPOR1/R2 expression in visceral epididymal adipose tissue (vEAT). It also lowered serum leptin (P < .05) and increased adiponectin levels. Furthermore, PNO supplementation increased P-AMPK/AMPK and P-AKT/AKT ratio and decreased the expression of FOXO-1 in both visceral epididymal and retroperitoneal adipose tissue (vEAT and vRPAT). Therefore, the present study showed that incorporation of PNO in the diet might prevent obesity and improve the metabolic inflammatory state in obesity by controlling the release of adipokines and proinflammatory cytokines. Comparative analysis between vEAT and vRPAT also revealed that vEAT is metabolically more active in combating obesity than vRPAT.