av P Björntorp · 1972 · Citerat av 318 — oxygen uptake, plasma lipids, glucose and lipid tolerance, and plasma insulin men were characterized by a small adipose tissue consisting of small fat cells, 

The Rho family member GTPase TC10 has been shown to play a role in insulin-stimulated glucose uptake and translocation of the glucose transporter GLUT4 in 3T3L1 adipocytes (5, 6). In this signaling cascade, the insulin receptor and TC10 reside constitutively in lipid raft microdomains of the plasma membrane.

In: Özcan S. (eds) Diabetes Mellitus. Methods in Molecular Biology™, vol 83. Shikonin stimulated glucose uptake and potentiated insulin-stimulated glucose uptake in a concentration-dependent manner in 3T3-L1 adipocytes. Stimulation of glucose uptake was also observed in rat primary adipocytes and cardiomyocytes. Resveratrol (Res) is a natural polyphenolic compound with anti-inflammatory and antioxidative effects.

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If you need insulin for diabetes, there’s good news: You have choices. There are five types of insulin. If you have to take insulin to treat diabetes, there’s good news: You have choices.There are five types of insulin. They vary by o People with diabetes need insulin treatment, usually intravenous injections. Insulin is a hormone produced in the pancreas to convert glucose (a type of sugar) in the blood into energy. After digesting food, glucose levels in the body rise, High insulin levels in your blood can lead to many serious health problems. Here are 14 diet and lifestyle changes you can make to reduce your insulin.

av A Green · 2014 · Citerat av 17 — Curcumin has been reported to inhibit insulin signaling and translocation of GLUT4 to the cell surface in 3T3-L1 adipocytes. inhibited both basal and insulin-stimulated glucose transport (2-deoxyglucose uptake), but had no 

J. (2003) 376, 625–632 (Printed in Great Britain) 625 Calpain facilitates GLUT4 vesicle translocation during insulin-stimulated glucose uptake in adipocytes David S. PAUL, Anne W Glucose uptake measured by flow cytometry is referred to the uptake of 1 glucose analog, 2-NBDG. Our results show that exposure of 3T3L1 and C2C12 cells to arsenic caused a dose-dependent reduction in glucose uptake in response to insulin stimulation (Figs.

Insulin resistance results in decreased insulin-stimulated glucose transport into skeletal muscle and adipocyte tissue . Keywords Glucose Uptake Chronic Hyperglycemia Newborn Calf Serum Basal Glucose Uptake Mature White Adipocyte

Without Dex treatment, the cellular glucose uptake was increased significantly in response of insulin stimulation (Fig. S1A). chemerin potentiated insulin-stimulated glucose uptake concom-itant with enhanced insulin signaling in the 3T3-L1 adipocytes. These data establish that chemerin is a novel adipokine that reg-ulates adipocyte function.

Effect of CETP on insulin-stimulated glucose uptake in adipocytes. Adipose tissue is an endocrine organ secreting factors that can both improve and impair insulin sensitivity. In general, well‐functioning adipose tissue secretes adipokines and other molecules with important regulatory effects such as leptin 34, adiponectin 35 and the recently described novel family of lipids, the FAHFAs 36. Furthermore, the data indicate that the cellular content of GLUT4 is the rate‐limiting factor in mediating maximal insulinstimulated glucose uptake in GLUT4(+/–) adipocytes.—Li, J., Houseknecht, K. L., Stenbit, A. E., Katz, E. B., Charron, M. J. Reduced glucose uptake precedes insulin signaling defects in adipocytes from heterozygous GLUT4 knockout mice.
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Similar to isoproterenol-medi-ated inhibition of insulin signaling, treating adipocytes with for-skolin, a potent activator of AC, inhibits insulin signaling (4, 5).

Here we describe the identification and characterization of BMP2 and BMP6 as new insulin-sensitizing growth factors in mature adipocytes. We Furthermore, the data indicate that the cellular content of GLUT4 is the rate‐limiting factor in mediating maximal insulinstimulated glucose uptake in GLUT4(+/–) adipocytes.—Li, J., Houseknecht, K. L., Stenbit, A. E., Katz, E. B., Charron, M. J. Reduced glucose uptake precedes insulin signaling defects in adipocytes from heterozygous Insulin resistance results in decreased insulin-stimulated glucose transport into skeletal muscle and adipocyte tissue .
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2015-09-01 · In addition, insulin-stimulated glucose uptake was significantly impaired in adipocytes isolated from AdipPanx1KO mice compared to adipocytes isolated from WT mice (Figure 2B). Since pharmacological as well as genetic inhibition of Panx1 in adipocytes resulted in blunted insulin-stimulated glucose uptake, we hypothesized that Panx1-mediated ATP release was responsible for the effect.

It increases AKT phosphorylation in the  av C Saloranta — Denna s.k. metabola resistens kan antingen vara hela förklaringen till ett insulinresistent tillstånd uptake and esterification in adipose tissue. Biochem Biophys  Within the adipocyte, insulin regulates: Glut4 expression, acetyl-CoA Insulin secretion and insulin sensitivity can be measured objectively following  Exercise training improves adipose tissue metabolism and vasculature regardless of baseline glucose tolerance and sex.

Insulin resistance results in decreased insulin-stimulated glucose transport into skeletal muscle and adipocyte tissue . Keywords Glucose Uptake Chronic Hyperglycemia Newborn Calf Serum Basal Glucose Uptake Mature White Adipocyte

Under insulin-resistant conditions, it is well known that insulin-stimulated glucose uptake is impaired, and many studies attribute this to a defect in Akt signaling. Insulin-resistance is the main cause of type 2 diabetes.

Since pharmacological as well as genetic inhibition of Panx1 in adipocytes resulted in blunted insulin-stimulated glucose uptake, we hypothesized that Panx1-mediated ATP release was responsible for the effect. Basal glucose uptake in adipocytes treated with 5, 10, or 20μM DIM significantly increased by ∼1.4‐, 1.8‐, and 3.2‐fold, respectively, compared with controls. In the absence of DIM, insulin‐stimulated glucose uptake of adipocytes was increased by approximately 1.8‐fold compared with the basal level. 2018-05-01 · Res increases glucose uptake of insulin-resistant 3T3-L1 adipocytes. We first established the insulin-resistant model in 3T3-L1 adipocytes treated with dexamethasone (Dex). Without Dex treatment, the cellular glucose uptake was increased significantly in response of insulin stimulation (Fig. S1A).