In the present study, we aimed to investigate whether chronic oral glutamine (Gln) supplementation may alter metabolic parameters and the inflammatory profile in overweight and obese humans as well as whether Gln may modulate molecular pathways in key tissues linked to the insulin action in rats. Thirty-nine overweight/obese volunteers received 30 g of Gln or alanine (Ala-control) for 14 days. Body weight (BW), waist circumference (WC), hormones, and pro-inflammatory markers were evaluated. To investigate molecular mechanisms, Gln or Ala was given to Wistar rats on a high-fat diet (HFD), and metabolic parameters, euglycemic hyperinsulinemic clamp with tracers, and Western blot were done. Gln reduced WC and serum lipopolysaccharide (LPS) in overweight volunteers. In the obese group, Gln diminished WC and serum insulin. There was a positive correlation between the reduction on WC and LPS. In rats on HFD, Gln reduced adiposity, improved insulin action and signaling, and reversed both defects in glucose metabolism in the liver and muscle. Gln supplementation increased muscle glucose uptake and reversed the increased hepatic glucose production, in parallel with a reduced glucose uptake in adipose tissue. This insulin resistance in AT was accompanied by enhanced IRS1 O-linked-glycosamine association in this tissue, but not in the liver and muscle. These data suggest that Gln supplementation leads to insulin resistance specifically in adipose tissue via the hexosamine pathway and reduces adipose mass, which is associated with improvement in the systemic insulin action. Thus, further investigation with Gln supplementation should be performed for longer periods in humans before prescribing as a beneficial therapeutic approach for individuals who are overweight and obese.

Inflammatory bowel disease (IBD) is a complex inflammatory disorder characterized by chronic and spontaneously relapsing inflammation of the gastrointestinal tract. IBD includes two idiopathic disorders: Crohn’s disease (CD) and ulcerative colitis (UC). In particular, UC causes inflammation and ulceration of the colon and rectum. There is no cure for UC. The pharmacological treatment is aimed at controlling and/or reducing the inflammatory process and promoting disease remission. The present study investigated the possible protective effects of soluble dietary fiber (SDF) isolated from yellow passion fruit peel in the dextran sulfate sodium‐ (DSS‐) induced colitis model in mice, induced by 5% of DSS. The animals were treated with SDF (10, 30, or 100 mg/kg (po)), and the disease activity index was monitored. Colon tissues were collected, measured, and prepared for oxidative stress, inflammation, and histology analysis. SDF improved body weight loss, colon length, and disease activity index and prevented colonic oxidative stress by regulating GSH levels and SOD activity. Furthermore, SDF reduced colonic MPO activity, TNF‐α, and IL‐1β levels and increased IL‐10 and IL‐6 levels. As observed by histological analysis, SDF treatment preserved the colonic tissue, the mucus barrier, and reduced inflammatory cell infiltration. Although this is a preliminary study, taken together, our data indicate that SDF may improve the course of DSS‐UC. More studies are needed to explore and understand how SDF promotes this protection.

Gastrointestinal mucositis is a serious and dose-limiting toxic side effect of oncologic treatment. Interruption of cancer treatment due to gastrointestinal mucositis leads to a significant decrease in cure rates and consequently to the deterioration of a patient’s quality of life. Natural polysaccharides show a variety of beneficial effects, including a gastroprotective effect. Treatment with soluble dietary fiber (SDF) from yellow passion fruit (Passiflora edulis) biomass residues protected the gastric and intestinal mucosa in models of gastrointestinal injury. In this study, we investigated the protective therapeutic effect of SDF on 5-FU-induced mucositis in male and female mice. Oral treatment of the animals with SDF did not prevent weight loss but reduced the disease activity index and preserved normal intestinal function by alleviating diarrhea and altered gastrointestinal transit. SDF preserved the length of the colon and histological damage caused by 5-FU. SDF significantly restored the oxidative stress and inflammation in the intestine and the enlargement and swelling of the spleen induced by 5-FU. In conclusion, SDF may be a promising adjuvant strategy for the prevention and treatment of intestinal mucositis induced by 5-FU.