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Pathophysiology of Heart Failure with Reduced Ejection Fraction
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Jacob Cao, John O'Sullivan, Sean Lal
Sodium-glucose transporter 2 (SGLT2) is a transmembrane protein located in the proximal convoluted tubules of nephrons for reabsorption of filtered glucose. Three large, randomized, placebo-controlled trials (EMPA-REG OUTCOME, CANVAS Program, DECLARE-TIMI 58) have demonstrated impressive reductions of ~30% in HF hospitalization following treatment with the SGLT2 inhibitors empagliflozin, canagliflozin, and dapagliflozin in type 2 diabetes patients (Figure 3.6 and Table 3.1).29–33 Similar results have been noted in the post-marketing study CVD-REAL of more than 300,000 patients, demonstrating a 39% lower risk of HF hospitalization in those taking SGLT2 inhibitors versus other glucose-lowering agents.34
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 cell and tissues
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Facilitated diffusion is a process in which molecules are assisted in moving down their concentration gradient across the plasma membrane. A good example of this facilitation is the movement of glucose molecules into the cell. There are receptor molecules on the surface of the cell membrane, which are activated by the attachment of insulin. Once the receptor is activated, it, in turn, activates the carrier molecules in the plasma membrane. The carrier molecules are specifically designed to interact with the glucose molecules. No extra energy is required because the carrier molecules are designed to move into the cell, where they connect with the glucose molecule. There are, in fact, two types of carrier, that operate like taxis. Some are waiting in the cell membrane (taxi rank) and others are cruising waiting to pick up free glucose molecules. If these transport molecules are missing or if they malfunction, glucose transport into the cells is reduced. The transport of glucose is also critically dependent on insulin being attached to the cell plasma membrane to enable the glucose transport to take place (see Figure 3.5).
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.
Kolaviron modulates dysregulated metabolism in oxidative pancreatic injury and inhibits intestinal glucose absorption with concomitant stimulation of muscle glucose uptake
Published in Archives of Physiology and Biochemistry, 2023
Veronica F. Salau, Ochuko L. Erukainure, Neil A. Koorbanally, Md. Shahidul Islam
To further buttress the inhibitory potential of kolaviron as an antidiabetic agent, the intestinal glucose absorption in rat jejunum and skeletal muscle glucose uptake were investigated. The rate of glucose absorption in the small intestine which is known to be highest at the joining of the duodenum to the jejunum has a major impact on postprandial glucose level (Chukwuma et al.2018). From our result (Figure 4), intestinal glucose absorption was strongly inhibited dose-dependently with increasing concentration of kolaviron as against the control which was not incubated with kolaviron. Muscle glucose uptake is actively involved in glucose homeostasis. Insulin, through the help of glucose transporter 4 (GLUT 4), stimulates uptake of glucose from the blood to target organs such as the muscle (Alvim et al.2015, Pereira et al.2017). However, skeletal muscle glucose uptake is impaired in the development and progression of type 2 diabetes as a result of insulin resistance which leads to sustained hyperglycaemia (Chukwuma et al.2018). In this study, the increased glucose uptake in muscles incubated with kolaviron (Figure 5) indicates the ability of the flavonoid to decrease hyperglycaemia. This corroborates its inhibitory property on carbohydrate digesting enzymes, thus confirming the antidiabetic potential of kolaviron.
Forkhead box C2 is associated with insulin resistance in gestational diabetes mellitus
Published in Gynecological Endocrinology, 2022
Jing Yang, Fen Liu, Yi Li, Dongbo Wu, Zhenhui Zhang, Sicen Chen, Mandan Deng, Chengying Yang, Jing Yang
Adiponectin is the most abundant peptide secreted by adipocytes that plays a vital role in preventing insulin resistance/diabetes. Recently, clinical studies have revealed that hypoadiponectinemia is associated with a marked increase in risk for development of GDM [8]. Adiponectin deficiency induces hyperglycemia and other metabolic defects of GDM in pregnant adiponectin gene knockout (Adipoq−/−) mice [9]. Glucose transporter-4 (GLUT4) is an essential glucose transporter in the skeletal muscle membrane and is an important factor of glucose intolerance. The overexpression of GLUT4 significantly improves insulin-signaling in GDM, leading to improved glycemic control and increased insulin secretion in spontaneous gestational diabetic C57BLKS/J Lepr(db/+) mice [10]. Forkhead box C2 (FOXC2) is a winged helix/forkhead transcription factor gene and plays an important role in adipocyte metabolism [11]. The human FOXC2 gene is located on chromosome 16q24.3, and the genetic variation of the FOXC2 gene is associated with triglyceride levels [12]. Reduced expression of FOXC2 and brown adipogenic genes such as MASK in human is associated with insulin resistance [13].