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Preventing, Treating, and Reversing Chronic Disease With Nutritional Interventions
Published in Gia Merlo, Kathy Berra, Lifestyle Nursing, 2023
Alexandra Lessem, Caroline Trapp
Type 2 DM is directly impacted by weight and nutrition status. Traditionally, diabetes was thought to develop from excess sugar and carbohydrate intake. Evidence now shows that in most cases sustained over-consumption of calories and subsequent growth in adipose tissue leads to type 2 DM. Insulin resistance in muscle tissue occurs long before diagnosed diabetes and has been shown to be due to dysfunctional glucose transporter protein type 4 (GLUT-4) function from excess adipose tissue and associated oxidative stress (Boden et al., 2015) as well as increased intramyocellular lipid droplets in the skeletal muscle cells (Meex et al., 2019). GLUT-4 is the primary membrane transport protein to allow glucose into muscle and adipose cells and is essential for glucose homeostasis (Vargas et al., 2021). When the peripheral cells begin to show insulin resistance, the body responds by increasing insulin production, which leads to increased fat in the liver and pancreas, eventually leading to beta cell destruction and need for exogenous insulin (Taylor et al., 2019). Through reversing this trend, largely through very calorie deficient diets, the cycle can be interrupted, and diabetes reversed (Taylor, 2008; Taylor et al., 2019).
Molecular sport nutrition
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Mark Hearris, Nathan Hodson, Javier Gonzalez, James P. Morton
At rest, the primary regulation of the location of GLUT4 is by insulin. In a fasted state when insulin concentrations are low, very little GLUT4 is found on the membrane of skeletal muscle (or adipose tissue) and the rate of glucose uptake into these tissues is low. After eating a meal containing carbohydrate or protein (such as that recommended in the pre-exercise meal), the rise in blood glucose and amino acid (AA) concentrations – combined with the release of some gut hormones – results in the release of insulin by the pancreas. Insulin is transported in the bloodstream and binds to the insulin receptor on muscle cells. Once insulin has bound to the insulin receptor on the muscle membrane, a cascade of insulin signalling begins, which stimulates the movement of GLUT4 from storage within the cell to the plasma membrane. By increasing the amount of GLUT4 at the muscle membrane, this allows more glucose to enter the cell (Figure 10.2A) which can then lead to glycogen storage.
Therapeutic Potential of Anthocyanin Against Diabetes
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Health Benefits of Secondary Phytocompounds from Plant and Marine Sources, 2021
Tawheed Amin, H. R. Naik, Bazila Naseer, Syed Zameer Hussain
Some drugs (thiazolidinediones and metformin) and several components of food may conceivably have antidiabetic effects [21, 97]. Dietary anthocyanin-rich bilberry (European blue berries) extract significantly activates AMPK in skeletal muscle and white adipose tissue. This activation thus increases the protein expression of GLUT4, improving the take-up of glucose into these cells or tissues through an insulin-dependent mechanism [102] thus prompting the decrease in hyperglycemia. Activated AMPK additionally results in the hindrance of glucose production, formation of fat and stimulation of fatty acid oxidation [105].
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.
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].