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Bacterial Endotoxin Activity in Human Serum Is Associated With Dyslipidemia, Insulin Resistance, Obesity, and Chronic Inflammation

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TLDR
In this paper, the authors investigated whether bacterial lipopolysaccharide (LPS) activity in human serum is associated with the components of the metabolic syndrome (MetS) in type 1 diabetic patients with various degrees of kidney disease and patients with IgA glomerulonephritis (IgAGN).
Abstract
OBJECTIVE To investigate whether bacterial lipopolysaccharide (LPS) activity in human serum is associated with the components of the metabolic syndrome (MetS) in type 1 diabetic patients with various degrees of kidney disease and patients with IgA glomerulonephritis (IgAGN) RESEARCH DESIGN AND METHODS Serum LPS activity was determined with the Limulus Amoebocyte Lysate chromogenic end point assay in type 1 diabetic patients with a normal albumin excretion rate ( n = 587), microalbuminuria ( n = 144), macroalbuminuria ( n = 173); patients with IgAGN ( n = 98); and in nondiabetic control subjects ( n = 345) The relationships of the LPS/HDL ratio and MetS-associated variables were evaluated with Pearson correlation RESULTS The MetS was more prevalent in type 1 diabetic patients (48%) than in patients with IgAGN (15%) Diabetic patients with macroalbuminuria had a significantly higher serum LPS/HDL ratio than patients with IgAGN In the normoalbuminuric type 1 diabetic group, patients in the highest LPS/HDL quartile were diagnosed as having the MetS three times more frequently than patients in the lowest quartile (69 vs 22%; P CONCLUSIONS High serum LPS activity is strongly associated with the components of the MetS Diabetic patients with kidney disease seem to be more susceptible to metabolic endotoxemia than patients with IgAGN Bacterial endotoxins may thus play an important role in the development of the metabolic and vascular abnormalities commonly seen in obesity and diabetes-related diseases

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Human gut microbiome: hopes, threats and promises

TL;DR: Recent evidence of the impact of the gut microbiota on metabolic disorders and focus on selected key mechanisms is discussed and the cases of the bacteria Prevotella copri and Akkermansia muciniphila will be discussed as key examples.
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Fetuin-A acts as an endogenous ligand of TLR4 to promote lipid-induced insulin resistance

TL;DR: It is shown that fetuin-A (FetA) could be this endogenous ligand for TLR4 and that it has a crucial role in regulating insulin sensitivity via Tlr4 signaling in mice, and may position FetA as a new therapeutic target for managing insulin resistance and type 2 diabetes.
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Systemic Effects of Inflammation on Health during Chronic HIV Infection

TL;DR: It is likely that knowledge gained on how inflammation affects health in HIV disease could have implications for the understanding of other chronic inflammatory diseases and the biology of aging.
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Microbiota and diabetes: an evolving relationship

TL;DR: As a ‘gut signature’ becomes more evident in T2D, a better understanding of the role of the microbiota in diabetes might provide new aspects regarding its pathophysiological relevance and pave the way for new therapeutic principles.
References
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Journal ArticleDOI

Homeostasis model assessment : insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man

TL;DR: The correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
Journal ArticleDOI

Metabolic endotoxemia initiates obesity and insulin resistance

TL;DR: It is concluded that the LPS/CD14 system sets the tone of insulin sensitivity and the onset of diabetes and obesity and lowering plasma LPS concentration could be a potent strategy for the control of metabolic diseases.
Journal ArticleDOI

The role of inflammatory cytokines in diabetes and its complications.

TL;DR: Although the precise role of inflammation in the development of diabetic microvascular diseases is still unclear, it is likely that inflammation induced by diabetes and insulin resistance can accelerate atherosclerosis in patients with diabetes.
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