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Insulin and Brain Reward Systems
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Brian C. Liu, Qingchen Zhang, Emmanuel N. Pothos
Insulin signaling in the brain is largely similar to insulin signaling in the periphery. The main difference seems to involve the downstream glucose transporters. In the periphery, the insulin signaling pathway results in the translocation of glucose transporter 4 (GLUT4) to the membrane in order to allow for glucose uptake from the bloodstream (46). In the brain, GLUT4 is not widely expressed and is primarily found in regions such as the hypothalamus and hippocampus (47, 48). Glucose uptake in the brain occurs through GLUT1, which is insulin-insensitive, in astrocytes and endothelial cells in the blood-brain barrier (49, 50).
The Working Rat Heart Preparation
Published in John H. McNeill, Measurement of Cardiac Function, 2020
Of course, any one of several standard balanced salt solutions can be used with this preparation. In practice, the type which seems to have gained the most favor in recent years is some version of Krebs-Henseleit (K-H) solution, varying in only minor respects from one laboratory to another. The formula we use is as follows10 (concentrations in millimolar): NaCl (120); KC1 (5.6); MgSO4 (0.65); NaH2PO4 (1.21); NaHCO3 (19 to 25); CaCl2 (1.8 to 2.4). The most common exogenous fuel is glucose, usually between 8 and 12 mM. Of course, any other soluble fuel, such as pyruvate, beta-hydroxybutyrate, or lactate, can be substituted or supplemented at the desired concentrations.8 When glucose is present, insulin is often added to enhance glucose uptake.11
Hypofibrinolysis and Hyperinsulinemia
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Stephen C.L. Gough, Irene Juhan-Vague
An insensitivity to the action of insulin, namely resistance to insulin-stimulated glucose uptake, has been found in the majority of patients with impaired glucose tolerance, type 2 diabetes mellitus, hypertriglyceridemia, hypertension, and obesity.2,3 These clinical and biological features are each independently associated with an increased risk for the development of coronary artery disease.4-7 Due to clustering of these features around insulin resistance and the ensuing hyperinsulinemia, Reaven hypothesized that resistance to insulin-stimulated glucose uptake may be involved in the etiology of type 2 diabetes mellitus, hypertension, and coronary artery disease.8
Antihyperglycemic effects of Lysiphyllum strychnifolium leaf extract in vitro and in vivo
Published in Pharmaceutical Biology, 2023
Arman Syah Goli, Vilasinee Hirunpanich Sato, Hitoshi Sato, Savita Chewchinda, Jiraporn Leanpolchareanchai, Jannarin Nontakham, Jantana Yahuafai, Thavaree Thilavech, Pongsatorn Meesawatsom, Metawee Maitree
Insulin mediates the mobility of the glucose transporter, GLUT4, to facilitate cellular glucose uptake. After insulin binds to the tyrosine kinase receptor, it induces the activation of protein-kinase B (Akt) and protein kinase C to accelerate the translocation of GLUT4 from the intracellular storage compartments to the plasma membrane (Bryant et al. 2002). Our study found that daily administration of the LS extract (1000 mg/kg) to STZ-NA-induced DM mice for 28 days decreased FBG by approximately 43%, and markedly enhanced serum insulin and GLUT4 concentrations compared to those in untreated DM mice. Therefore, the LS extract may boost insulin production and stimulate the mobilization of GLUT4 to the membranes of skeletal muscle cells to facilitate glucose uptake for energy utilization.
Talin1 regulates glucose metabolism and endometrial receptivity via GLUT-4 in patients with polycystic ovary syndrome and insulin resistance
Published in Gynecological Endocrinology, 2023
Jingjing Li, Saiqiong Chen, Rongyan Qin, Xin Liu, Li Fan, Mengjun Wei, Jiajia Wei, Jiajing Lin, Fengque Zheng
As a glucose transporter, GLUT-4 is involved in rapid glucose uptake by various cells to maintain glucose homeostasis. Previous studies have suggested that abnormal endometrial GLUT4 expression may be responsible for increased miscarriage rates in women with type 2 diabetes or PCOS [30–32]. Several studies have found reduced mRNA and protein levels of GLUT-4 in the endometrium of PCOS patients compared to control patients[33–35], whereas GLUT4 mRNA and protein levels in the endometrium of PCOS-IR patients were reduced to a greater extent [36, 37]. Therefore, abnormal GLUT-4 expression may be an important mechanism of endometrial IR in patients with PCOS. GLUT4 plays a key role in endometrial receptivity. Long et al. [38] showed that inhibiting GLUT4 expression in the mouse uterus affects embryo development and implantation. Our study found low GLUT4 expression in the endometrium of both PCOS-IR patients and PCOS-IR mice, similar to the results of previous studies. The Tlian1 expression in the endometrium was negatively correlated with FBG, while GLUT4 was involved in glucose uptake. In vitro experiments also revealed that silencing and overexpression of Talin1 affected GLUT4 expression and that Talin1 protein and GLUT4 protein interacted, suggesting that Talin1 may affect glucose metabolism and endometrial tolerance in patients with PCOS-IR by regulating GLUT4.
The role of resveratrol in diabetes and obesity associated with insulin resistance
Published in Archives of Physiology and Biochemistry, 2023
Mustafa Hoca, Eda Becer, Hafize Seda Vatansever
Resveratrol also reduced fasting hyperinsulinemia and promoted intracellular glucose transport in high-cholesterol-fructose diet fed rats (Deng et al.2008). Additionally, resveratrol induced insulin receptor phosphorylation and also glucose transporter type 4 (GLUT4) translocation to muscle plasma membrane in insulin resistant animals. This leads to glucose uptake and increases glucose utilisation in cells (Deng et al.2008, Tan et al. 2012). Apart from metabolic changes in skeletal muscle, resveratrol also induced beneficial effects in the liver. In animal models, resveratrol elevated the expression and phosphorylation of SIRT1 and AMPK in the liver. Thus, resveratrol can increase the sensitivity of insulin and repair an impaired insulin-signalling by the SIRT1-AMPK pathway (Chen et al.2012, Do et al.2012, Guo et al.2014, Zhu et al. 2014). In summary, these results show that resveratrol has beneficial effects by improving the insulin level and sensitivity by changing SIRT1 and AMPK protein expressions.