Tea, a popular beverage made from leaves of the plant Camellia sinensis, has been shown to reduce body weight, alleviate metabolic syndrome, and prevent diabetes and cardiovascular diseases in animal models and humans. Such beneficial effects have generally been observed in most human studies when the level of tea consumption was 3 to 4 cups (600–900 mg tea catechins) or more per day. Green tea is more effective than black tea. In spite of numerous studies, the fundamental mechanisms for these actions still remain unclear. From a review of the literature, we propose that the two major mechanisms are: 1) decreasing absorption of lipids and proteins by tea constituents in the intestine, thus reducing calorie intake; and 2) activating AMPK by tea polyphenols that are bioavailable in the liver, skeletal muscle, and adipose tissues. The relative importance of these two mechanisms depends on the types of tea and diet consumed by individuals. The activated AMPK would decrease gluconeogenesis and fatty acid synthesis and increase catabolism, leading to body weight reduction and MetS alleviation. Other mechanisms and the health relevance of these beneficial effects of tea consumption remain to be further investigated.

The study of brown adipose tissue (BAT) in human weight regulation has been constrained by the lack of a noninvasive tool for measuring this tissue and its function in vivo. Existing imaging modalities are nonspecific and intrinsically insensitive to the less active, lipid-rich BAT of obese subjects, the target population for BAT studies. We demonstrate noninvasive imaging of BAT in mice by hyperpolarized xenon gas MRI. We detect a greater than 15-fold increase in xenon uptake by BAT during stimulation of BAT thermogenesis, which enables us to acquire background-free maps of the tissue in both lean and obese mouse phenotypes. We also demonstrate in vivo MR thermometry of BAT by hyperpolarized xenon gas. Finally, we use the linear temperature dependence of the chemical shift of xenon dissolved in adipose tissue to directly measure BAT temperature and to track thermogenic activity in vivo.MRI | hyperpolarized 129 Xe | brown adipose tissue | thermometry | FDG-PET

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Scope Human breast milk has been shown to prevent necrotizing enterocolitis (NEC). Although exosomes have been identified in breast milk, their function and components have not been fully addressed. This study is conducted to elucidate the differences in peptidomic complexities between preterm and term milk exosomes. Methods and results Breast milk samples are collected from healthy lactating mothers who have delivered term and preterm infants. Exosomes are separated and quantified. The protective effects of purified exosomes against NEC are investigated both in vitro and in vivo. The peptidomic complexities in term and preterm milk exosomes are analyzed by iTRAQ LC‐MS/MS to screen differentially expressed exosomal peptides. Preterm milk exosomes administration significantly enhances proliferation and migration of intestinal epithelial cells compared with term milk exosomes. A total of 70 peptides are found to be significantly modulated in preterm milk samples compared to term milk samples. Of these, 47 peptides are upregulated, and 23 peptides are downregulated. Bioinformatics analysis suggests several potential regulatory roles of the altered peptides in intestinal epithelial cell function. Conclusion These results reveal the differences for the first time in peptidomic complexities between preterm and term milk exosomes. Milk exosome administration might be a promising prevention for NEC.

A Mn3O4/Ni foam electrode prepared by a facile method exhibits excellent electrocatalytic performance for the oxygen evolution reaction.

Aims Diabetic nephropathy (DN) is a major diabetic complication characterized by mesangial proliferation and glomerular hypertrophy. MicroRNAs might play an important role in these pathological processes. The aim of this study is to examine the possible association of miR-34a as one of the microRNAs with DN and underlying mechanisms in vitro and in vivo. Methods According to previous results of microarray which compared the different microRNAs between diabetic and normal control mice, miR-34a was chosen and its expression was detected by qRT-PCR. Cell viability was then assessed using Cell Counting Kit-8 (CCK8) and 5-ethynyl-20-deoxyuridine (EDU) incorporation. Antagomir was injected in db/db mice to down regulate miR-34a. Average diameter of glomeruli was analyzed by periodic acid-Schiff (PAS) stain of kidney. Luciferase gene report assay was then performed to identify the target gene of miR-34a. Additional immunoblotting and immunohistochemical analyses were implemented to verify the expression level of growth arrest-specific 1 (GAS1). Results MiR-34a expression level was increased under high glucose condition in vitro and in vivo. Down-regulation of miR-34a inhibits mice mesangial cells (MMCs) proliferation in vitro and alleviates glomerular hypertrophy in vivo. GAS1 was proved to be the target of miR-34a through luciferase report. Moreover, up-regulation of GAS1 expression was observed in the presence of miR-34a antagomir as compared withmiR-34a antagomir-NC in high-glucose-treated MMCs and db/db mice, respectively. Conclusions MiR-34a regulated mesangial proliferation and glomerular hypertrophy by directly inhibiting GAS1 in early DN.

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