Nutrition (Burbank, Los Angeles County, Calif.) · 2019
Zinc supplementation improves glucose homeostasis in patients with β-thalassemia major complicated with diabetes mellitus: A randomized controlled trial.
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод в очереди
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Matter Randa Mahmoud, Elbarbary Nancy Samir, Ismail Eman Abdel Rahman, Darwish Yasser Wagih, Nada Ahmed Shafik, Banoub Veronia Philip
Аннотация
OBJECTIVES: The development of abnormal glucose tolerance in β-thalassemia major (β-TM) is associated with alterations in the oxidant-antioxidant status. Zinc is an antioxidant and an essential element for insulin synthesis, storage, and secretion. This randomized controlled trial assessed the effect of oral zinc supplementation on glucose homeostasis in pediatric β-TM patients complicated with diabetes mellitus (DM).
METHODS: Eighty patients were randomly assigned into two groups: an intervention group that received oral zinc in a dose of 40 mg/d for 12 wk and a placebo group. Hemolysis markers, serum ferritin, fasting blood glucose (FBG), fructosamine, fasting C-peptide, urinary albumin excretion (UAE), and serum zinc levels were assessed. Homeostasis model assessment insulin resistance index (HOMA-IR) was calculated.
RESULTS: Baseline clinical and laboratory parameters were consistent among both groups. Baseline zinc levels were decreased in both groups compared with control values. After 12 wk, supplementation with zinc for the intervention group resulted in a significant decrease in lactate dehydrogenase, serum ferritin, FBG, fructosamine, HOMA-IR, and UAE, whereas fasting C-peptide was higher compared with baseline levels and with the placebo group (P < 0.05). Baseline serum zinc was negatively correlated to FBG (r = -0.534, P < 0.001) and fructosamine (r = -0.555, P < 0.001) but positively correlated to fasting C-peptide (r = 0.777, P = 0.002).
CONCLUSIONS: Zinc supplementation as an adjuvant therapy in β-TM patients with DM reduced iron burden, decreased hyperglycemia, increased insulin secretion, and improved glycemic control without any adverse effects.
METHODS: Eighty patients were randomly assigned into two groups: an intervention group that received oral zinc in a dose of 40 mg/d for 12 wk and a placebo group. Hemolysis markers, serum ferritin, fasting blood glucose (FBG), fructosamine, fasting C-peptide, urinary albumin excretion (UAE), and serum zinc levels were assessed. Homeostasis model assessment insulin resistance index (HOMA-IR) was calculated.
RESULTS: Baseline clinical and laboratory parameters were consistent among both groups. Baseline zinc levels were decreased in both groups compared with control values. After 12 wk, supplementation with zinc for the intervention group resulted in a significant decrease in lactate dehydrogenase, serum ferritin, FBG, fructosamine, HOMA-IR, and UAE, whereas fasting C-peptide was higher compared with baseline levels and with the placebo group (P < 0.05). Baseline serum zinc was negatively correlated to FBG (r = -0.534, P < 0.001) and fructosamine (r = -0.555, P < 0.001) but positively correlated to fasting C-peptide (r = 0.777, P = 0.002).
CONCLUSIONS: Zinc supplementation as an adjuvant therapy in β-TM patients with DM reduced iron burden, decreased hyperglycemia, increased insulin secretion, and improved glycemic control without any adverse effects.