brefeldin a/aptaukošanās

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Chemical Inducers of Obesity-Associated Metabolic Stress Activate Inflammation and Reduce Insulin Sensitivity in 3T3-L1 Adipocytes.

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Ielogoties Reģistrēties

Obesity is accompanied by dyslipidemia, hypoxia, endoplasmic reticulum (ER) stress, and inflammation, representing the major risk factor for the development of insulin resistance (IR) and type 2 diabetes. We modeled these conditions in cultured 3T3-L1 adipocytes and studied their effect on insulin

Serum chemerin levels vary with time of day and are modified by obesity and tumor necrosis factor-{alpha}.

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Chemerin is an adipokine with important regulatory roles in adipogenesis. In humans, serum total chemerin (i.e. prochemerin plus chemerin) levels are positively associated with body mass index and metabolic syndrome. However, the mechanisms that increase serum chemerin concentration are unknown. We

Tumor necrosis factor-alpha contributes to obesity-related hyperleptinemia by regulating leptin release from adipocytes.

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Cytokines, in particular tumor necrosis factor-alpha (TNF-alpha), have significant effects on energy metabolism and appetite although their mechanisms of action are largely unknown. Here, we examined whether TNF-alpha modulates the production of leptin, the recently identified fat-specific energy

TERT enhances the survival rate of human fibroblasts under endoplasmic reticulum, Golgi apparatus, and lysosomal stresses.

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OBJECTIVE The exposure of organelles, such as the endoplasmic reticulum (ER), Golgi apparatus (GA), and lysosomes, to stress activates death mechanisms. Recently, telomerase reverse transcriptase (TERT) has been shown to be involved in cell survival. However, the relationship between TERT and the

Optimized protocol for the preparation of single cells from cutaneous wounds for flow cytometric cell sorting and analysis of macrophages

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The incidence of chronic, non-healing skin wounds is accelerating, largely due to the epidemic of obesity-related Type 2 diabetes. Abnormal inflammation in wounds contributes to delayed healing. During wound repair, blood monocytes are recruited into the wound bed where they differentiate into

Transporter regulator RS1 (RSC1A1) coats the trans-Golgi network and migrates into the nucleus.

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The product of gene RSC1A1, named RS1, is involved in transcriptional and posttranscriptional regulation of sodium-d-glucose cotransporter SGLT1, and removal of RS1 in mice led to an increase of SGLT1 expression in small intestine and to obesity (Osswald C, Baumgarten K, Stümpel F, Gorboulev V,

Molecular and cellular mechanisms of adipose secretion: comparison of leptin and angiotensinogen.

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Besides their function of lipid storage, the adipose cells secrete a number of proteins of physiopathological importance. To get further insights into this function, which remains poorly characterized, we sought to compare the mechanisms and regulation of secretion of two individual proteins in the

Identification of a new secretory factor, CCDC3/Favine, in adipocytes and endothelial cells.

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The vascular system secretes many bioactive factors. In a gene chip database, we searched for novel genes with signal sequences that are specifically expressed in murine aorta, and focused on one gene previously named CCDC3 (NCBI nucleotide entry NM_028804), and we designated as Favine

Visfatin is released from 3T3-L1 adipocytes via a non-classical pathway.

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Visfatin is a secretory protein which exerts insulin mimetic and proinflammatory effects, also functioning as an intracellular enzyme to produce NAD. Plasma visfatin levels and visfatin mRNA expression in adipose tissues are increased in obese subjects. Visfatin does not have a decent cleavable

Endoplasmic reticulum stress induces leptin resistance.

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Leptin is an important circulating signal for inhibiting food intake and body weight gain. In recent years, "leptin resistance" has been considered to be one of the main causes of obesity. However, the detailed mechanisms of leptin resistance are poorly understood. Increasing evidence has suggested

Lipolysis response to endoplasmic reticulum stress in adipose cells.

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In obesity and diabetes, adipocytes show significant endoplasmic reticulum (ER) stress, which triggers a series of responses. This study aimed to investigate the lipolysis response to ER stress in rat adipocytes. Thapsigargin, tunicamycin, and brefeldin A, which induce ER stress through different

TNF-α up-regulates protein level and cell surface expression of the leptin receptor by stimulating its export via a PKC-dependent mechanism.

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Increasing evidence suggests that inflammation/cytokines may modulate hypothalamic responses to leptin, which is a key regulator of energy homeostasis and inflammatory/stress responses. We investigated a possible role of TNF-α, a key early mediator of inflammation, in regulating the expression and

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