Gut microbiota-directed intervention with high-amylose maize ameliorates metabolic dysfunction in diet-induced obese mice.

Obesity is a chronic disease that may lead to the development of metabolic diseases, cardiovascular diseases, and cancers and has been predicted to affect one billion adults by 2030. Owing to the pivotal role of the gut microbiota in health, including metabolism and energy homeostasis, dietary fiber, the primary energy resource for the gut microbiota, not only helps reduce appetite and short-term food intake but also modulates the structure of the gut microbiota. In this study, we investigated whether high-amylose maize (HAM), with a particular amount of dietary fiber, improves dysmetabolism and gut microbiota dysbiosis in diet-induced obese mice. Promisingly, the HAM dietary intervention not only reduced body weight gain, adipocyte hypertrophy, and dyslipidemia but also mitigated non-alcoholic fatty liver disease, insulin resistance, impaired glucose tolerance, and inflammation in the liver and epididymal white adipose tissues in high-fat diet (HFD)-fed obese mice. In addition, the HAM dietary intervention ameliorated gut microbiota dysbiosis in HFD-fed mice. Changes in families, genera, and species of gut biota that have a relative abundance of 0.01% in at least one group were scrutinized. At the species level, HAM dietary intervention increased Bifidobacterium pseudolongum, Bifidobacterium animalis, Bifidobacterium bifidum, and Lactobacillus paraplantarum and decreased Streptococcus agalactiae, Mucispirillum schaedleri, and Alistipes indistinctus. This change in the gut microbiota driven by the HAM diet was strongly associated with obesity-related indices, highlighting the nutraceutical potential of HAM for improving overall metabolic health. Taken together, this study demonstrates the potential of the HAM diet for mediating metabolic syndrome and gut microbiota dysbiosis.

ε-Viniferin and α-viniferin alone or in combination induced apoptosis and necrosis in osteosarcoma and non-small cell lung cancer cells.

This study investigated the effects and molecular mechanisms of ε-viniferin and α-viniferin in non-small cell lung cancer cell line A549, melanoma cell line A2058, and osteosarcoma cell lines HOS and U2OS. Results showed ε-viniferin having antiproliferative effects on HOS, U2OS, and A549 cells. Compared with ε-viniferin at the same concentration, α-viniferin had higher antiproliferative effects on HOS cells, but not the same effect on U2OS and A549 cells. Lower dose combination of α-viniferin and ε-viniferin had more synergistic effects on A549 cells than either drug alone. α-Viniferin induced apoptosis in HOS cells by decreasing expression of phospho-c-Jun-N-terminal kinase 1/2 (p-JNK1/2) and increasing expression of cleaved Poly (ADP-ribose) polymerase (PARP), whereas α-viniferin in combination with ε-viniferin induced apoptosis in A549 cells by decreasing expression of phospho-protein kinase B (p-AKT) and increasing expression of cleaved PARP and cleaved caspase-3. ε-Viniferin and α-viniferin have not been studied using in vivo tumor models for cancer. This research is the first showing that ε-viniferin treatment resulted in significant inhibition of tumor growth in A549-cell xenograft-bearing nude mice compared with the control group. Consequently, ε-viniferin and α-viniferin may prove to be new approaches and effective therapeutic agents for osteosarcoma and lung cancer treatment.

Ugonin J improves metabolic disorder and ameliorates nonalcoholic fatty liver disease by regulating the AMPK/AKT signaling pathway.

Closely associated with visceral obesity, hepatic steatosis resulting from non-alcoholic fatty liver disease (NAFLD) exacerbates insulin resistance. Developing effective drugs to treat NAFLD is imperative. Here, we investigated the pharmacological mechanism of ugonin J (UJ) in controlling metabolic disorder and ameliorating NAFLD pathophysiology in diet-induced obese mice. The effects of UJ were assessed in 5-week-old C57BL/6 J mice fed a high-fat diet (HFD) for 12 weeks. UJ treatment averted HFD-induced body weight gain by reducing fat deposition in adipose tissues and reduced HFD-induced hyperlipidemia and hepatic inflammation. UJ also improved HFD-induced glucose tolerance and insulin resistance. Moreover, the mode of action of UJ was analyzed in palmitate (PA)-induced steatotic human HuS-E/2 hepatocytes and in hyperglycemia-simulating rat BRIN-BD11 pancreatic ß cells. In PA-induced steatotic human hepatocytes, UJ treatment promoted lipid clearance via pAMPK, pACC and CPT-1 upregulation and SREBP-1c downregulation. Interestingly, UJ upregulated Akt activity in hepatocytes and increased insulin secretion from ß cells in acute insulin secretion tests. Taken together, UJ improved adipocyte hypertrophy, hyperinsulinemia, hyperglycemia, hyperlipidemia and fat deposition in livers. UJ also reduced fatty acid accumulation by modulating key metabolic regulators. Our findings demonstrated the therapeutic potential of UJ for the treatment of NAFLD and diet-induced metabolic disorders.

Comparison of Demographic Parameters and Predation Rates of Orius strigicollis (Hemiptera: Anthocoridae) Fed on Eggs of Tetranychus urticae (Acari: Tetranychidae) and Cadra cautella (Lepidoptera: Pyralidae).

Orius strigicollis (Poppius) is an anthocorid bug with high foraging ability on thrips as well as on mites, and the bug has been considered as a potential biological control agent in Taiwan. Life table and predation studies of O. strigicollis fed on Cadra cautella (Walker) and Tetranychus urticae (Koch) eggs were conducted at 25 ± 1°C. Data were analyzed and compared using TWOSEX-MSChart and CONSUME-MSChart software. O. strigicollis fed on eggs of C. cautella, a substitute prey, showed significantly higher survival rate and developmental rate than individuals fed on their natural prey, T. urticae eggs. The fecundity of O. strigicollis fed on C. cautella eggs was, on average, 13.2 times higher than that of those fed on T. urticae eggs, despite of the fact that during the entire nymphal stage, the consumption rate of O. strigicollis on T. urticae eggs was ca. 9 times higher than on almond moth eggs The conversion rate (i.e., number of prey eggs needed to produce one predator egg) for this predatory bug reared on T. urticae eggs and almond moth eggs were 604.6 and 6.0, respectively, indicating that almond moth eggs served as an effective alternative prey for ensuring the predator's reproduction. This is the first study pertaining to the population parameters and predation rates of O. strigicollis using the age-stage two-sex approach to describe differences between O. strigicollis populations reared on natural and alternative preys. This information may be useful in mass rearing programs and field application involving this biological control agent.