Τρίτη 1 Μαρτίου 2022

Asiatic acid improves high-fat-diet-induced osteoporosis in mice via regulating SIRT1/FOXO1 signaling and inhibiting oxidative stress

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Histol Histopathol. 2022 Mar 1:18446. doi: 10.14670/HH-18-446. Online ahead of print.

ABSTRACT

Asiatic acid can attenuate osteoporosis through suppressing adipogenic differentiation and osteoclastic differentiation. Oxidative stress enhances osteoclastic differentiation but represses osteogenic differentiation to promote osteoporosis. However, the role and mechanism of asiatic acid in osteoporosis have not been reported. Firstly, mice were fed with high-fat-diet (HFD) with or without asiatic acid for 16 weeks. Data from an automatic biochemical analyzer showed that HFD induced down-regulation of high-density lipoprotein (HDL) and an increase of serum levels of triglyceride (TG), total cholesterol (TC) and low-density lipoprotein (LDL). However, asiatic acid administration attenuated the decrease of HDL and increase of serum TG, TC and LDL in osteoporotic mice. Secondly, HFD induced high levels of malondialdehyde (MDA) and reactive oxyg en species (ROS), low levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in osteoporotic mice. However, the levels of MDA, ROS, SOD and GSH-Px in osteoporotic mice were reversed by asiatic acid administration. (this section is unclear and requires revision) Asiatic acid administration reduced expression of c-telopeptide of type 1 collagen (CTX-1), enhanced alkaline phosphatase (ALP) and procollagen type 1 N-terminal propeptide (P1NP) in HFD-induced osteoporotic mice. (this section is unclear and requires revision) Thirdly, asiatic acid promoted calcium deposition in bone marrow cells and osteogenic differentiation in osteoporotic mice, but decreased ALP in bone marrow cells. Lastly, asiatic acid enhanced SIRT1 and nuclear FOXO1 (Nu-FOXO1) expression, while it reduced Acetyl FOXO1 (Ac-FOXO1) in osteoporotic mice. In conclusion, asiatic acid might inhibit oxidative stress and promote osteogenic differentiation through activating SIRT1/FOXO1 to attenuate HFD-induc ed osteoporosis in mice.

PMID:35229281 | DOI:10.14670/HH-18-446

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Graves' disease in children and adolescents in Iceland

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Laeknabladid. 2022 Mar;108(3):123-129. doi: 10.17992/lbl.2022.03.680.

ABSTRACT

INTRODUCTION: Graves' disease is an autoimmune disease in which autoantibodies cause an increase in the production of thyroid hormones, and is the most common cause of thyrotoxicosis in children. Symptoms in children are often more obscure than in adults. The aim of the study is to assess the incidence of Graves' disease in children and adolescents in Iceland over the span of two decades (2001-2021), and furthermore to investigate if the incidence rate has increased, as well as to describe treatment options and disease recurrence.

MATERIAL/METHODS: This retrospective descriptive study included all children diagnosed with Graves' disease in the years 2001-2021 in Iceland. Information was obtained from the Directorate of Health's drug database and from ICD-10 diagnoses at Landspítali - The National University Hospital.

RESULTS: In total, 57 children and adolescents were diagnosed with Graves', the overall incidence rate was 3.5/100,000 person-years. Gender ratio was 1:2.7 (male : female) and the mean age at diagnosis was 13.6 for boys and 13.9 years for girls. Of those 12 individuals currently receiving drug therapy (21.8%), four patients have had disease relapse. Thirteen patients reached an euthyroid state with medication (23.7%), 25 received treatment with radioactive iodine (45.5%) and 5 underwent surgery (9.1%). Boys were more likely to relapse. Disease recurrence w as 31.8%.

CONCLUSION: The incidence of Graves' disease did not increase during the study period. The disease was more common in girls, although the gender ratio was lower than expected. Antithyroid drugs were the first choice in treatment and radioactive iodine was the most common permanent treatment option. Disease recurrence was common. A possible relationship between the duration of the original drug therapy and disease recurrence should be investigated.

PMID:35230257 | DOI:10.17992/lbl.2022.03.680

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