Taste sensitivity throughout age and the relationship with the sleep quality

Objective: The aim of the present study was to evaluate taste sensitivity and sleep pattern throughout age. Methods: Thirty-five male adults aged (25.05±0.71 years), and twenty- four older adults (68.92 ± 6.43 years) were selected and submitted to sleep evaluation (Pittsburgh Sleep Quality Index and Epworth Sleepiness Scale), as well as taste sensitivity. Taste sensitivity was evaluated using three dilutions and the different concentrations were presented for the four basic flavors (salty, sweet, bitter and sour). These samples were encoded with three digits and randomly presented to the participants in 50 mL plastic cups. Results: In both groups, sleep quality was poor (PSQI >5). Older adults presented a negative effect to identify sweet and salty taste and, in this population, sleep time was associated with sweet taste perception. Discussion: We may suggest that aging may cause changes in taste sensitivity, as well as total sleep time was observed to be a significant predictor of sweet taste. Sleep may play an important role in taste sensitivity, although the mechanisms are still unknown. Thus, the results of this research may contribute to the emergence of new studies that seek to better understand this relationship of sleep quality as taste sensitivity

Oral Glutamine Supplementation Reduces Obesity, Pro-Inflammatory Markers, and Improves Insulin Sensitivity in DIO Wistar Rats and Reduces Waist Circumference in Overweight and Obese Humans

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