lysozyme/obesity

Background & aims: Several proteins of the innate immune system are known to be deregulated with insulin resistance. We here aimed to investigate the relationship among circulating lysozyme (both plasma concentration and activity) and

Complex clinical and laboratory research of nonspecific immunobiological reactivity was conducted in 86 children (35 with diabetes mellitus, 25 with obesity, and 26 healthy children), aged from 3 to 14 years. Lysozyme activity and complement titre were studied during the disease. Reduced reactive

In the pathophysiological context of obesity, oral exposure to dietary fat can modulate lipid digestion and absorption, but underlying in-mouth mechanisms have not been clearly identified. Therefore, we tested the hypothesis that salivary components related to dietary fat sensitivity would differ

Diabetes in the non-obese diabetic (NOD) mouse is a multigenic autoimmune disease and is possibly controlled by three recessive loci, including one that is linked to the major histocompatibility complex (MHC). The first external domain of the Class II MHC I-A beta chain in these mice is unique and

BACKGROUND Lysozyme (LZ), a host-defense protein, contains an 18 amino-acid domain with high affinity binding for sugar-derived proteins or lipids, called advanced glycation endproducts (AGE), that are implicated in diabetes- and age-dependent complications (DC). METHODS A) The effects of LZ on AGE-

Aspects of humoral, secretory and cell-mediated immunologic status were studied in a group of 22 adults with severe, uncomplicated obesity. Normal concentrations of serum immunoglobulins (IgG, IgA, IgM, IgD) and complement components (C3, C4) were found. Levels of secretory IgA and lysozyme in the

Some obese subjects overeat lipid-rich foods. The origin of this eating behavior is unknown. We have here tested the hypothesis that these subjects could be characterized by an impaired fatty taste sensitivity linked to a change in the gustatory papillae microbial and salivary environment. The

Obesity is associated with gut microbiota dysbiosis, disrupted intestinal barrier and chronic inflammation. Given the high and increasing prevalence of obesity worldwide, anti-obesity treatments that are safe, effective and widely available would be beneficial. We examined whether the medicinal

The intestinal microbiota is increasingly acknowledged to play a crucial role in the development of obesity. A shift in intestinal microbiota composition favouring the presence of Firmicutes over Bacteroidetes has been observed in obese subjects. A similar shift has been reported in mice with

Chronic low-grade inflammation of adipose tissue plays a crucial role in the pathophysiology of obesity. Immunohistological microscopic analysis in obese fat tissue has demonstrated the infiltration of several immune cells such as macrophages, but dynamics of immune cells have not been fully

Msi1 (Musashi 1) is regarded as a marker for neural and intestinal epithelial stem cells. However, it is still unclear whether Msi1-positive cells derived from mouse embryonic stem cells have the ability to differentiate into neural or intestinal epithelial cells. A pMsi1-GFP (green fluorescent

B cells have an important pathogenic role in the development of type 1 diabetes in the non-obese diabetic (NOD) mouse. We have previously reported that NOD mice display an increased percentage of TACIhigh -expressing B cells compared with C57BL/6 mice and this trait is linked to chromosomes 1 and 8.

Sleep-disordered breathing (SDB) is a risk factor for cardiovascular disease (CVD). The underlying pathogenesis is not clear. In patients with obstructive sleep apnoea syndrome (OSAS) elevated levels of inflammatory markers, such as C-reactive protein (CRP), interleukin-6 (IL-6) and tumour necrosis

BACKGROUND Nasal instillation is an effective method for inducing antigen-specific immune tolerance. However, it is not clear how a tolerization scheme established in one mouse strain will perform when used in a mouse of a different haplotype. OBJECTIVE To compare the antigen-specific recall