Wheat‐ghretropins: novel ghrelin‐releasing peptides derived from wheat protein

Ghrelin is an endogenous orexigenic hormone mainly produced by stomach cells and is reported to influence appetite, gastrointestinal motility and growth hormone secretion. We observed that enzymatic digest of wheat gluten stimulated ghrelin secretion from mouse ghrelinoma 3-1, a ghrelin-releasing cell line. Further on, we characterized the ghrelin-releasing peptides present in the digest by comprehensive peptide analysis using liquid chromatography-mass spectrometry and structure-activity relationship. Among the candidate peptides, we found that SQQQQPVLPQQPSF, LSVTSPQQVSY and YPTSL stimulated ghrelin release. We then named them wheat-ghretropin A, B and C, respectively. In addition, we observed that wheat-ghretropin A increased plasma ghrelin concentration and food intake in mice after oral administration. Thus, we demonstrated that wheat-ghretropin stimulates ghrelin release both in vitro and in vivo. To the best of our knowledge, this is the first report of a wheat-derived exogenous bioactive peptide that stimulates ghrelin secretion

BRASSICA オヨビ RAPHANUS ゾク ノ ニホンサン ザイライ ヒンシュ ノ アブラナカ コクハンビョウキン ALTERNARIA BRASSICAE ニ タイスル テイコウセイ ヒョウカ

BrassicaおよびRaphanus属5種138品種を用い,アブラナ科黒斑病菌A. brassicaeによる接種試験を行った。実生葉へA. brassicaeを接種し,4日後の接種部位あるいは接種葉の状態から,発病度を5段階(0-4)で評価した。その結果,無病徴(発病度0)から,極めて軽微な病徴(発病度1),接種部位における病斑(発病度2),接種部位を越えた病斑(発病度3),接種葉が枯れる(発病度4)までの幅広い病徴発現の差が認められた。発病度0はB. rapa Pekinensis Groupより2品種,B. rapa Rapifera GroupおよびR. sativusよりそれぞれ1品種ずつの計4品種で見出された。A total of 138 cultivar seedlings of Brassica spp. and Raphanus sativus were inoculated with the fungal pathogen Alternaria brassicae. Four days after inoculation, disease severity on the seedlings was judged with five criteria (0-4) according to the incidence of lesions. Lesions of various levels, from undetectable (disease severity 0) until withering (disease severity 4), were shown on the seedling depending on the cultivars. As disease severity 0, two cultivars from B. rapa Pekinensis Group, and one cultivar each from B. rapa Rapifera Group and R. sativus were found

Empagliflozin induces the transcriptional program for nutrient homeostasis in skeletal muscle in normal mice

Abstract Sodium-glucose cotransporter 2 inhibitors (SGLT2i) improve heart failure (HF) outcomes across a range of patient characteristics. A hypothesis that SGLT2i induce metabolic change similar to fasting has recently been proposed to explain their profound clinical benefits. However, it remains unclear whether SGLT2i primarily induce this change in physiological settings. Here, we demonstrate that empagliflozin administration under ad libitum feeding did not cause weight loss but did increase transcripts of the key nutrient sensors, AMP-activated protein kinase and nicotinamide phosphoribosyltransferase, and the master regulator of mitochondrial gene expression, PGC-1α, in quadriceps muscle in healthy mice. Expression of these genes correlated with that of PPARα and PPARδ target genes related to mitochondrial metabolism and oxidative stress response, and also correlated with serum ketone body β-hydroxybutyrate. These results were not observed in the heart. Collectively, this study revealed that empagliflozin activates transcriptional programs critical for sensing and adaptation to nutrient availability intrinsic to skeletal muscle rather than the heart even in normocaloric condition. As activation of PGC-1α is sufficient for metabolic switch from fatigable, glycolytic metabolism toward fatigue-resistant, oxidative mechanism in skeletal muscle myofibers, our findings may partly explain the improvement of exercise tolerance in patients with HF receiving empagliflozin

Runx2 Represses Myocardin-Mediated Differentiation and Facilitates Osteogenic Conversion of Vascular Smooth Muscle Cells▿

Phenotypic plasticity and the switching of vascular smooth muscle cells (SMCs) play a critical role in atherosclerosis. Although Runx2, a key osteogenic transcription factor, is expressed in atherosclerotic plaques, the molecular mechanisms by which Runx2 regulates SMC differentiation remain unclear. Here we demonstrated that Runx2 repressed SMC differentiation induced by myocardin, which acts as a coactivator for serum response factor (SRF). Myocardin-mediated induction of SMC gene expression was enhanced in mouse embryonic fibroblasts derived from Runx2 null mice compared to wild-type mice. Forced expression of Runx2 decreased the expression of SMC genes and promoted osteogenic gene expression, whereas the reduction of Runx2 expression by small interfering RNA enhanced SMC differentiation in human aortic SMCs. Runx2 interacted with SRF and interfered with the formation of the SRF/myocardin ternary complex. Thus, this study provides the first evidence that Runx2 inhibits SRF-dependent transcription, as a corepressor independent of its DNA binding. We propose that Runx2 plays a pivotal role in osteogenic conversion tightly coupled with repression of the SMC phenotype in atherosclerotic lesions