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Mannose-binding lectin in obesity with different degrees of metabolic syndrome abnormalities: association with atherogenic and metabolic traits.
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OBJECTIVE
In subjects with metabolic syndrome (MetS) endothelial dysfunction is a very consistent finding. Processes leading to endothelial dysfunction and atherosclerosis involve the altered control of subclinical inflammation by innate immune defenses that possibly include mannose-binding lectin
Mannose-binding lectin is required for the effective clearance of apoptotic cells by adipose tissue macrophages during obesity.
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Obesity is accompanied by the presence of chronic low-grade inflammation manifested by infiltration of macrophages into adipose tissue. Mannose-binding lectin (MBL), a soluble mediator of innate immunity, promotes phagocytosis and alters macrophage function. To assess the function of MBL in the
Circulating levels of insulin-like growth factor-II/mannose-6-phosphate receptor in obesity and type 2 diabetes.
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OBJECTIVE
The extracellular domain of the insulin-like growth factor II/mannose-6-phosphate receptor (IGF-II/M6P-R) is present in the circulation, but its relationship with plasma IGF-II is largely unknown. As IGF-II appears to be nutritionally regulated, we studied the impact of obesity, type 2
Mannose Alters Gut Microbiome, Prevents Diet-Induced Obesity, and Improves Host Metabolism.
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Mannose is an important monosaccharide for protein glycosylation in mammals but is an inefficient cellular energy source. Using a C57BL6/J mouse model of diet-induced obesity, we show that mannose supplementation of high-fat-diet-fed mice prevents weight gain, lowers adiposity, reduces liver
Hyperexpression of N-acetylglucosaminyltransferase-III in liver tissues of transgenic mice causes fatty body and obesity through severe accumulation of Apo A-I and Apo B.
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N-Acetylglucosaminyltransferase (GnT)-III catalyzes the attachment of an N-acetylglucosamine (GlcNAc) residue to mannose in beta(1-4) configuration in the region of N-glycans and forms a bisecting GlcNAc. To investigate the pathophysiological role of dysregulated glycosylation mediated by aberrantly
Repeat treatment of obese mice with BRL 49653, a new potent insulin sensitizer, enhances insulin action in white adipocytes. Association with increased insulin binding and cell-surface GLUT4 as measured by photoaffinity labeling.
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(+/-)-5-([4-[2-Methyl-2(pyridylamino)ethoxy]phenyl]methyl) 2,4-thiazolidinedione (BRL 49653) is a new potent antidiabetic agent that improves insulin sensitivity in animal models of NIDDM. In C57BL/6 obese (ob/ob) mice, BRL 49653, included in the diet for 8 days, improved glucose tolerance. The
Plasma mannose-binding lectin is stimulated by PPARα in humans.
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The peroxisome proliferator activated receptor-α (PPARα) is a major transcriptional regulator of lipid metabolism in liver and represents the molecular target for hypolipidemic fibrate drugs. Effects of PPARα on lipid metabolism are partially mediated by circulating proteins such as FGF21 and
The effect of weight loss on serum mannose-binding lectin levels.
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BACKGROUND
Serum levels of the mannose-binding lectin (MBL), which is an activator of the complement system, have been considered as a pathogenic factor in a broad range of diseases, and means of modulating MBL are therefore being evaluated. In this study we examine the effects of weight loss on MBL
The plant mannose-binding lectin NTL preserves cord blood haematopoietic stem/progenitor cells in long-term culture and enhances their ex vivo expansion.
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Ex vivo expansion of haematopoietic stem and progenitor cells in cytokine combinations is effective in promoting differentiation and proliferation of multilineage progenitor cells, but often results in reduction of self-renewable stem cells. This study investigated the effect of a mannose-binding
Distinct Gut Microbiota and Serum Metabolites in Response to Weight Loss Induced by Either Dairy or Exercise in a Rodent Model of Obesity.
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Energy imbalance is a primary cause of obesity. While the classical approach to attenuate weight gain includes an increase in energy expenditure through exercise, dietary manipulation such as the inclusion of dairy products has also been proven effective. In the present study, we explored the
[Association between mannose-binding-lectin gene and type 2 diabetic patients in Chinese population living in the northern areas of China].
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OBJECTIVE
To investigate whether the mannose-binding-lectin 2 (MBL2) gene was associated with type 2 diabetes in the populations living the northern part of China.
METHODS
The study involved 318 type 2 diabetic patients and 448 normoglycemic controls. The variances of rs1800450, rs1800451 and
High-fat diet-induced plasma protein and liver changes in obese rats can be attenuated by melatonin supplementation.
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Obesity triggers changes in protein expression in various organs that might participate in the pathogenesis of obesity. Melatonin has been reported to prevent or attenuate such pathological protein changes in several chronic diseases. However, such melatonin effects on plasma proteins have not yet
Antioxidation, hepatic- and renal-protection of water-extractable polysaccharides by Dictyophora indusiata on obese mice.
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The present work aimed to investigate the antioxidation, hepatic- and renal-protection of water-extractable polysaccharides (WPS) by Dictyophora indusiata fruiting body on high-fat emulsion-induced obese mice. The structural analysis indicated that WPS was the α-configurational heteropolysaccharide
Role of CC chemokine receptor 2 in bone marrow cells in the recruitment of macrophages into obese adipose tissue.
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The MCP-1 (monocyte chemoattractant protein-1)/CCR2 (CC motif chemokine receptor-2) pathway may play a role in macrophage infiltration into obese adipose tissue. Here we investigated the role of CCR2 in the recruitment of bone marrow-derived macrophages into obese adipose tissue in vitro and in
A good sugar, d-mannose, suppresses autoimmune diabetes.
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It is well known that too much sugar uptake causes many health problems, including diabetes and obesity (Lustig et al. in Nature 482:27-29, 2012). However, a team of researchers led by Dr. Wanjun Chen of the National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of
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