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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Abdominal Fat, Aging, Animals, Blood Glucose, Dietary Sucrose, Glucose, Male, Mice, Oxidative Stress, Porphobilinogen Synthase, Random Allocation, Thiobarbituric Acid Reactive Substances, Weight Gain.
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Does long-term sucrose and glucose consumption decrease the delta-aminolevulinate dehydratase activity in mice? Context: This study evaluated the long-term effects of high-glucose (GLU) and high-sucrose (SUC) diets on the development of obesity, abdominal fat deposition, glucose intolerance, oxidative stress and effects on delta-aminolevulinate dehydratase (delta-ALA-D) activity in various organs. In particular, the effect of aging on these parameters was evaluated. Mice were assigned to a baseline, control, or experimental group. The control group was provided with tap water and experimental groups with solutions of glucose or sucrose for 30 wk. To verify the effect of aging, young mice (baseline group, 8 wk old) were compared with aged animals (control and experimental groups, 38 wk old). Consumption of GLU or SUC diets caused increases in body weight, abdominal fat index, and fasting plasma glucose levels. A positive correlation was observed between the abdominal fat index and fasting glucose levels. There was a significant increase in levels of thiobarbituric acid-reactive species (TBARS) and a significant decrease in delta-ALA-D activity in various tissues of GLU and SUC feeding mice. Importantly, the dithiothreitol-induced enzymatic reactivation in the GLU and SUC groups was significantly higher than in the control group, and in the aged group it was significantly higher than in the baseline group. After 30 wk, the experimental groups had a decrease in delta-ALA-D activity and an increase in TBARS levels in relation to the baseline group.
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Alterations in the activity of the delta-ALA-D found in this work demonstrate the possible contributions of hyperglycemia and aging for protein oxidation, leading to impairment of its biologic function. Final Decision: yes