Acute changes in the metabolome following resistance exercise combined with intake of different protein sources (cricket, pea, whey).

INTRODUCTION: Separately, both exercise and protein ingestion have been shown to alter the blood and urine metabolome. This study goes a step further and examines changes in the metabolome derived from blood, urine and muscle tissue extracts in response to resistance exercise combined with ingestion of three different protein sources. METHODS: In an acute parallel study, 52 young males performed one-legged resistance exercise (leg extension, 4 × 10 repetitions at 10 repetition maximum) followed by ingestion of either cricket (insect), pea or whey protein (0.25 g protein/kg fat free mass). Blood and muscle tissue were collected at baseline and three hours after protein ingestion. Urine was collected at baseline and four hours after protein ingestion. Mixed-effects analyses were applied to examine the effect of the time (baseline vs. post), protein (cricket, pea, whey), and time x protein interaction. RESULTS: Nuclear magnetic resonance (NMR)-based metabolomics resulted in the annotation and quantification of 25 metabolites in blood, 35 in urine and 21 in muscle tissue. Changes in the muscle metabolome after combined exercise and protein intake indicated effects related to the protein source ingested. Muscle concentrations of leucine, methionine, glutamate and myo-inositol were higher after intake of whey protein compared to both cricket and pea protein. The blood metabolome revealed changes in a more ketogenic direction three hours after exercise reflecting that the trial was conducted after overnight fasting. Urinary concentration of trimethylamine N-oxide was significantly higher after ingestion of cricket than pea and whey protein. CONCLUSION: The blood, urine and muscle metabolome showed different and supplementary responses to exercise and ingestion of the different protein sources, and in synergy the summarized results provided a more complete picture of the metabolic state of the body.

Transcriptome and metabolome changes induced by bitter melon (Momordica charantia)- intake in a high-fat diet induced obesity model.

Background and aim: Metabolic syndrome (MetS) is a complex disease of physiological imbalances interrelated to abnormal metabolic conditions, such as abdominal obesity, type II diabetes, dyslipidemia and hypertension. In the present pilot study, we investigated the nutraceutical bitter melon (Momordica charantia L) -intake induced transcriptome and metabolome changes and the converging metabolic signaling networks underpinning its inhibitory effects against MetS-associated risk factors. Experimental procedure: Metabolic effects of lyophilized bitter melon juice (BMJ) extract (oral gavage 200 mg/kg/body weight-daily for 40 days) intake were evaluated in diet-induced obese C57BL/6J male mice [fed-high fat diet (HFD), 60 kcal% fat]. Changes in a) serum levels of biochemical parameters, b) gene expression in the hepatic transcriptome (microarray analysis using Affymetrix Mouse Exon 1.0 ST arrays), and c) metabolite abundance levels in lipid-phase plasma [liquid chromatography mass spectrometry (LC-MS)-based metabolomics] after BMJ intervention were assessed. Results and conclusion: BMJ-mediated changes showed a positive trend towards enhanced glucose homeostasis, vitamin D metabolism and suppression of glycerophospholipid metabolism. In the liver, nuclear peroxisome proliferator-activated receptor (PPAR) and circadian rhythm signaling, as well as bile acid biosynthesis and glycogen metabolism targets were modulated by BMJ (p < 0.05). Thus, our in-depth transcriptomics and metabolomics analysis suggests that BMJ-intake lowers susceptibility to the onset of high-fat diet associated MetS risk factors partly through modulation of PPAR signaling and its downstream targets in circadian rhythm processes to prevent excessive lipogenesis, maintain glucose homeostasis and modify immune responses signaling.

The Functional Analysis of Selenium-Related Genes and Magnesium-Related Genes in the Gene Expression Profile Microarray in the Peripheral Blood Mononuclear Cells of Keshan Disease.

Keshan disease (KD) is an endemic cardiomyopathy with high mortality. Selenium (Se) deficiency is closely related to KD, while magnesium (Mg) plays many critical roles in the cardiovascular function. The molecular mechanism of KD pathogenesis is still unclear. Until now, we have not found any studies investigating the association between Se- or Mg-related genes and KD. In this study, oligonucleotide microarray analysis was used to identify the differentially expressed genes in the peripheral blood mononuclear cells between KD patients and normal controls. Next, human metabolome database (HMDB) was used to screen Se- and Mg-related genes. Function classification, gene pathway, and interaction network of Se- and Mg-related genes in KD peripheral blood mononuclear cells were defined by FunRich (functional enrichment analysis tool). Among 83 differentially expressed genes, five Se-related (DIO2, GPX1, GPX2, GPX4, and GPX7) and five Mg-related (ACSL6, EYA4, IDH2, PPM1A, and STK11) genes were recognized from HMDB. Two significant biological processes (energy pathways and metabolism), one molecular function (peroxidase activity), one biological pathway (glutathione redox reactions I), and one gene interaction network were constituted from Se-related and Mg-related genes. Se-related gene DIO2 and Mg-related genes STK11 and IDH2 may have key roles in the myocardial dysfunction of KD. However, we still have not obtained any interaction between Se-related gene and Mg-related gene. The interactions between RPS6KB1, PTEN, ATM, HSP90AA1, SNRK, PRKAA2, SMARCA4, HSPA1A, and STK11 may play important roles in the abnormal cardiac function of KD.