proteinase/obesity

BACKGROUND The development of obesity has been suggested to involve plasminogen activator inhibitor-1 (PAI-1) and tissue inhibitor of proteinases-1 (TIMP-1). Plasma PAI-1 is elevated in obesity. A low-glycemic-index (LGI) diet may have a beneficial effect on obesity through a decrease in plasma

OBJECTIVE We hypothesized that proteinase-activated receptor-2 (PAR2)-mediated vasorelaxation in murine aorta tissue can be due in part to the release of adipocyte-derived relaxing factors (ADRFs). METHODS Aortic rings from obese TallyHo and C57Bl6 intact or PAR2-null mice either without or with

Type 1 diabetes is considered to be an autoimmune disease in which T cells attack pancreatic islet cells. Impaired glucose tolerance with type 2 diabetes has been classified as an obesity-associated metabolic syndrome. However, recent studies have revealed that type 2 diabetes is an autoinflammatory

Failure to inhibit hepatic gluconeogenesis is a major mechanism contributing to fasting hyperglycemia in type 2 diabetes and, along with steatosis, is the hallmark of hepatic insulin resistance. Obesity is associated with chronic inflammation in multiple tissues, and hepatic inflammation is

Recent studies suggest that proteolytic enzymes located within the glomerulus are involved in the degradation of extracellular matrix components. In the present investigation glomerular proteinase activities were followed in a variety of non-immune-mediated renal diseases as well as during different

The objective of this research is to determine the action of the nucleotide oligomerization domain-like receptors containing pyrin domain 3 (NLRP3) inflammasome in the obesity paradox of rats with ventilator-induced lung injury (VILI). Twenty-four (average weight: 250 ± 20 g) pathogen-free adult

The obese Zucker rat is a classic model of non-immune-mediated spontaneous focal glomerulosclerosis. An early morphological hallmark of glomerular damage in the obese Zucker rat is a mesangial expansion, which precedes and mediates the development of glomerular damage in these animals. This study

Human diabetes mellitus (IDDM; type I diabetes) is a T cell-mediated disease that is closely modeled in non-obese diabetic (NOD) mice. The pathogenesis of IDDM involves the transmigration of autoimmune T cells into the pancreatic islets and the subsequent destruction of insulin-producing beta cells.

Adipose tissue development is associated with angiogenesis, adipogenesis and extracellular matrix degradation. The class of matrix metalloproteinases contributes to these processes, but little information is available on the role of individual proteinases. We report that stromelysin-2 (MMP-10)

The obese Zucker rat is a classic model of non-immune mediated spontaneous focal glomerulosclerosis. An important initiating hallmark of glomerulosclerosis in this model is mesangial matrix expansion. Fibronectin, a highly biologically active glycoprotein, is a normal constituent of mesangial

The obese Zucker rat develops non-immune-mediated spontaneous focal glomerulosclerosis. Mesangial matrix expansion is an important initiating hallmark of such glomerular damage and fibronectin is a normal constituent of mesangial extracellular matrix. Using a quantitative method based on enzyme

Because hyperlipidemia and macrophage influx appear to play a key role in the genesis of renal glomerulosclerosis, this study examined the temporal relationship between hyperlipidemia (triglycerides and cholesterol), mononuclear cell influx, changes in glomerular structure, and expansion of the

Mast cells are crucial for the development of allergic and anaphylactic reactions, but they are also involved in acquired and innate immunity. Increasing evidence now implicates mast cells in inflammatory diseases through activation by non-allergic triggers such as neuropeptides and cytokines. This

Activation of inflammatory pathways is known to accompany development of obesity-induced non-alcoholic fatty liver disease (NAFLD), insulin resistance and type 2 diabetes. In addition to caspase-1, the neutrophil serine proteases proteinase 3, neutrophil elastase and cathepsin G are able to process