Publications by authors named "Fanjie Zhang"

Introduction: Gut microbes and their metabolites play crucial roles in the pathogenesis of diabetic kidney disease (DKD). However, which one and how specific gut-derived metabolites affect the progression of DKD remain largely unknown.

Objectives: This study aimed to investigate the potential roles of indole-3-propionic acid (IPA), a microbial metabolite of tryptophan, in DKD.

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Background:  We aimed to investigate the role and mechanism of β-hydroxybutyrate dehydrogenase 1 (Bdh1) in regulating macrophage oxidative stress in diabetes-induced atherosclerosis (AS).

Methods:  We performed immunohistochemical analysis of femoral artery sections to determine differences in Bdh1 expression between normal participants, AS patients, and patients with diabetes-induced AS. Diabetic mice and high-glucose (HG)-treated Raw264.

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Chronic hyperglycemia-induced impairment of angiogenesis is important in diabetic foot ulcer (DFU). Additionally, the stimulator of interferon gene (STING), which is a key protein in innate immunity, mediates palmitic acid-induced lipotoxicity in metabolic diseases through oxidative stress-induced STING activation. However, the role of STING in DFU is unknown.

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The current guidelines recommend that people consume 2 or more servings of fat-rich fish per week to obtain enough omega-3 (ω-3) polyunsaturated fatty acids to prevent cardiovascular events. However, the cardiovascular benefits of ω-3 polyunsaturated fatty acids in patients with diabetes are unclear, and related large-scale trials have produced conflicting results. We aimed to perform a meta-analysis of all randomized controlled trials that attempted to assess the effects of ω-3 fatty acid supplementation on cardiovascular outcomes in patients with diabetes.

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Background: Chronic hyperglycemia-induced inflammation is recognized as the most important pathophysiological process in diabetic kidney disease (DKD). As maresin 1 (MaR1) is an extensive anti-inflammatory lipid mediator, the present study investigated the protective role of MaR1 in the pathogenesis of DKD and its clinical relevance.

Methods: Serum MaR1 concentrations were analyzed in 104 subjects with normal glucose tolerant, type 2 diabetes (T2DM), or DKD.

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The vitamin D analog ED-71 (eldecalcitol) has been shown to be superior to calcitriol and its precursor alfacalcidol in maintaining or increasing bone mass in women and animal models with osteoporosis. The mechanism for the greater effectiveness of ED-71 is unknown. In the present study, we tested the hypothesis that the higher activity of ED-71 is due to its higher affinity for the serum vitamin D binding protein (DBP) by comparing the activities of orally administered ED-71, calcitriol and 22-oxacalcitriol (OCT) in wild type (WT) and DBP-ablated (DBPko) mice.

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Article Synopsis
  • ED-71, a vitamin D analog approved for osteoporosis treatment in Japan, significantly enhances phosphate absorption in the intestines, showing an 8-fold increase compared to no effect from 1,25(OH)2D(3).
  • This increased absorption is linked to a 24-fold rise in sodium-dependent phosphate transporter type IIb (NaPi-IIb) mRNA in the duodenum, indicating a strong induction of this transporter by ED-71.
  • Unlike 1,25(OH)2D(3), which was ineffective in raising NaPi-IIb levels, ED-71's superior potency is attributed to its higher and longer-lasting blood levels, suggesting potential for treating phosphate-wasting disorders.
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The sigma-2 receptor, whose gene remains to be cloned, has been validated as a biomarker for tumour cell proliferation. Here we report the use of a novel photoaffinity probe, WC-21, to identify the sigma-2 receptor-binding site. WC-21, a sigma-2 ligand containing both a photoactive azide moiety and a fluorescein isothiocyanate group, irreversibly labels sigma-2 receptors in rat liver; the membrane-bound protein was identified as PGRMC1 (progesterone receptor membrane component 1).

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Background: Accelerated glucose uptake for anaerobic glycolysis is one of the major metabolic changes found in malignant cells. This property has been exploited for imaging malignancies and as a possible anticancer therapy. The nonmetabolizable glucose analog 2-deoxyglucose (2 DG) interferes with glucose metabolism leading to breast cancer cell death.

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Most cancer deaths are a consequence of resistance to conventional chemotherapy and radiation therapy. This may be attributable to unique phenotypic characteristics of solid tumors. We have exploited two well-described characteristics of solid tumors commonly associated with treatment failure, high glucose use and hypoxia, to design a unique therapy based on the selective accumulation of two cytotoxic compounds, 2-deoxyglucose (2-DG) and copper(II)diacetyl-bis(N(4)-methylthiosemicarbazone) ((64)Cu-ATSM).

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Exposure to ionizing radiation is believed to cause cell injury via the production of free radicals that are thought to induce oxidative damage. It has been proposed that exposure to agents that enhance oxidative stress-induced injury by disrupting thiol metabolism may sensitize cells to the cytotoxic effects of ionizing radiation. Recently, it has been shown that glucose deprivation selectively induces cell injury in transformed human cells via metabolic oxidative stress (J.

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