{"title":"Molecular Basis of Blood Glucose Regulation","authors":"Asma Ahmed, Noman Khalique","doi":"10.5772/intechopen.89978","DOIUrl":"https://doi.org/10.5772/intechopen.89978","url":null,"abstract":"Blood glucose level is regulated by multiple pancreatic hormones, which regulate it by different pathways in normal and abnormal conditions by expressing or suppressing multiple genes or molecular or cellular targets. Multiple synthetic drugs and therapies are used to cure glucose regulatory problems, while many of them are used to cure other health issues, which arise due to disturbance in blood glucose regulations. Many new approaches are used for the development of phytochemical-based drugs to cure blood glucose regulation problems, and many of the compounds have been isolated and identified to cure insulin resistance or regulate beta cell function or glucose absorption in the guts or GLP-1 homoeostasis or two/more pathways (e.g., either cure hyperglycemia or raise insulin resistance or cure pancreatic beta cell regeneration or augmentation of GLP-1, production of islet cell, production and increased insulin receptor signaling and insulin secretion or decreased insulin tolerance or gluconeogenesis and insulin-mimetic action or production of α -glucosidase and α -amylase inhibitor or conserve islet mass or activate protein kinase A (PKA) and extracellular signal regulated kinases (ERK) or activate AMPK and reduce insulin sensitivity or suppress α -glucosidase activity and activate AMPK and downstream molecules or prevents cell death of pancreatic β -cell and activates SIRT1 or lower blood glucose due to their insulin-like chemical structures or decrease lipid peroxidation.","PeriodicalId":109929,"journal":{"name":"Blood Glucose Levels","volume":"31 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"117139980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Symptoms of Hypoglycaemia","authors":"P. Loumpardia, M. Huda","doi":"10.5772/intechopen.88674","DOIUrl":"https://doi.org/10.5772/intechopen.88674","url":null,"abstract":"Hypoglycaemia is common in clinical practice for people with diabetes. However, the symptoms can vary between individuals and at different stages of their condition. Moreover, several factors influence symptoms experienced by people with diabetes, and many are amenable to intervention. Symptoms are commonly neuroglycopenic or neurogenic in aetiology, and these lead to different clusters of symptoms. Certain patient groups such as the elderly and pregnant women are particularly susceptible to hypoglycaemia. In this chapter, we describe the physiology and pathophysiology behind the symptoms of hypoglycaemia, with reference to current knowledge from neuroimaging studies, and outline potential interventions to modify or restore hypoglycaemia symptoms.","PeriodicalId":109929,"journal":{"name":"Blood Glucose Levels","volume":"2 4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123635932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Carbohydrate Metabolism in Hypoglycemia","authors":"M. L. Kennedy, M. A. Campuzano-Bublitz","doi":"10.5772/INTECHOPEN.88362","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.88362","url":null,"abstract":"Hypoglycemia is generated by mechanisms directly related to an increase in insulin secretion, by metabolic disorders that require increased glucose consumption or by a deficient metabolic production of glucose by the body. Mechanisms include high glucose intake, increased dose of oral hypoglycemic, exogenous administration of insulin, metabolic hepatic conditions that lead to an increase in the production of amino acids, growing tumors, and in diabetic pregnant woman with abnormal increase in glucose and amino acids that end up producing insulin hypersecretion in the newborn. Work that requires high glucose expenditure or reduction of insulin antagonist, such as cortisol and glucagon, ends up in hypoglycemia. Finally, hypoglycemia is generated by metabolic deficit in pathophysiological situations such as defects in enzymatic systems, alcoholic hepatitis, and insufficient nutrition. The most characteristic symptoms include bulimia, fits of sweating, and tremors due to a strong activation of the sympathetic system. Obviously, the CNS is strongly affected by the lack of glucose, which is even more complicated because also hypoglycemia leads to a situation of decreased lipolysis and ketone bodies that finally seriously compromise the supply of energy to the nervous system, producing losses of consciousness, spasms, and even irreversible brain damage.","PeriodicalId":109929,"journal":{"name":"Blood Glucose Levels","volume":"62 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115043395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hypoglycemia: Essential Clinical Guidelines","authors":"Thenmozhi Paluchamy","doi":"10.5772/INTECHOPEN.86994","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.86994","url":null,"abstract":"Hypoglycemia is the acute complication of diabetes mellitus and the commonest diabetic emergency and is associated with considerable morbidity and mortality. It can be caused by too much insulin intake or oral hypoglycemic agents, too little food, or excessive physical activity. The level of glucose that produces symptoms of hypoglycemia varies from person to person and varies for the same person under different circumstances. It characterized by sweating, tremor, tachycardia, palpitation, nervousness, hunger, confusion, slurred speech, emotional changes, double vision, drowsiness, sleeplessness, and often self-diagnosed which may leads to serious symptoms of seizure, cognitive impairment, coma and death. The immediate treatment of hypoglycemia should be known by all the diabetic patients, so that need for hospitalization could be avoided. Hypoglycemia and its severity can be prevented by early recognition of hypoglycemia risk factors, self-monitoring of blood glucose, selection of appropriate treatment regimens, appropriate educational programs for healthcare professionals. The major challenges of the treatment of hypoglycemia are good glycemic control, minimize the risk of hypoglycemia and thereby minimize long-term complications. Hence there is an urgent need to understand the clinical spectrum and burden of hypoglycemia so that adequate control measures can be implemented against this life-threatening complication.","PeriodicalId":109929,"journal":{"name":"Blood Glucose Levels","volume":"55 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129179124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Luiz Augusto da Silva, Jéssica Wouk, V. M. R. Weber
{"title":"Cardiovascular and Biochemical Responses in Exercise Recuperation in Diabetic Rats","authors":"Luiz Augusto da Silva, Jéssica Wouk, V. M. R. Weber","doi":"10.5772/INTECHOPEN.79084","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.79084","url":null,"abstract":"The objective of this study was to assess the cardiovascular and biochemical responses during aerobic exercise recuperation in diabetic rats. There were utilized 12 animals, of 60 days, divided in two groups: control and diabetic. On the test day, the animals performed a 60 minutes’ session of predominantly aerobic exercise, using an overload of 6% of their body’s weight. After and before the exercise, the animals had their systolic blood pressure (SBP) and heart rate (HR), lactate, glycerol and glucose measured. The animals were trained during 30 days by swimming tank, with an extra weight equivalent to 4% extra weight a 40-min session. A decrease in glucose value occurred in the diabetic animals after exercising, as well as an increase of lactate in the same group. 1’, 3’, 5’ and 7’ after the exercise, a significant reduction of HR in the diabetic group was noticed when compared with the control group, such behavior was also observed with double product (DP) together with SBP values 1’, 3’ and 5’ after the exercise. The diabetic animals’ recovery has been possibly affected by a reduction of blood flow and a reduction of energetic substrates contribution, as well as lactate clearance.","PeriodicalId":109929,"journal":{"name":"Blood Glucose Levels","volume":"229 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122903704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Effect of Ramadan Fasting on Metabolic Syndrome (MetS)","authors":"K. Aljaloud","doi":"10.5772/intechopen.89333","DOIUrl":"https://doi.org/10.5772/intechopen.89333","url":null,"abstract":"The effect of Ramadan fasting on most of the metabolic syndrome (MetS) markers is still controversial. However, most of the available evidences showed positive effect on most of the MetS markers. In general, Ramadan fasting may help to reduce the risk of MetS. Nevertheless, most of the positive results seem to be impermanent and reading many variables (MetS markers) return to the previous reading after few weeks (~3–4 weeks). Therefore, intermittent fasting such as Ramadan fasting could be one of the cure alternatives especially in people with MetS, cardiovascular or metabolic diseases with considering their physician supervision. Again, more evidences are recommended to clarify the controversial issues related to the role of Ramadan fasting on MetS markers.","PeriodicalId":109929,"journal":{"name":"Blood Glucose Levels","volume":"179 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116161522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Introductory Chapter: Glucose Transporters","authors":"L. Szablewski","doi":"10.5772/INTECHOPEN.82263","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.82263","url":null,"abstract":"The major source of energy for mammalian cells is glucose. Glucose derived from the diet and synthesized within the body is transported from the circulation into target cells. The transfer of glucose across the plasma membrane is necessary. Cell membrane is composed by lipid bilayer, which is hydrophobic. Glucose has hydrophilic nature. Therefore, cell membranes act as barriers to most molecules. For water molecules and a few other small molecules, such as oxygen and carbon dioxide, the lipid bilayer is permeable. These molecules move spontaneously down their concentration gradient by diffusion. For cations such as K+, Na+, and Ca2+; anions such as Cl and HCO3; and hydrophilic molecules and macromolecules such as proteins and RNA, lipid bilayer is impermeable. Therefore, these molecules and ions need specific transport system. There are two general classes of membrane transporters: channels and carriers. Glucose transporters belong to the major facilitator superfamily (MFS). MFS contains 74 families of membrane transporters including more than 10,000 members. These transporters transport variety of molecules. Glucose as well as other monosaccharides cannot penetrate the lipid bilayer because they are hydrophilic in nature; therefore, they require specific carrier proteins to undergo diffusion through the bilayer. In humans, there are three families of genes that encode for glucose transporters: SLC2A, SLC5A, and SLC50A [1]. Glucose is transported across the cell membranes and tissue barriers by a sodium-independent glucose transporter (facilitated transport, GLUT proteins, and SLC2 genes), sodium-dependent glucose symporters (secondary active transport, SGLT proteins, and SLC5 genes), and glucose uniporter—SWEET protein (SLC50 genes). Most cells express more than one kind of glucose transporters. However, these membrane carrier proteins are called glucose transporters; they are involved in the transport of several different molecules, not just glucose.","PeriodicalId":109929,"journal":{"name":"Blood Glucose Levels","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126446865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Świderska, Justyna Strycharz, Adam Wróblewski, J. Szemraj, J. Drzewoski, A. Śliwińska
{"title":"Role of PI3K/AKT Pathway in Insulin-Mediated Glucose Uptake","authors":"E. Świderska, Justyna Strycharz, Adam Wróblewski, J. Szemraj, J. Drzewoski, A. Śliwińska","doi":"10.5772/INTECHOPEN.80402","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.80402","url":null,"abstract":"Glucose uptake is regulated by several mechanisms, where insulin plays the most prominent role. This powerful anabolic hormone regulates the transport of glucose into the cell through translocation of glucose transporter from an intracellular pool to the plasma membrane mainly in metabolically active tissues like skeletal muscles, adipose tissue, or liver (GLUT4). This translocation occurs through multiple steps of PI3K/AKT signaling pathway. In this chapter, we will focus on molecular events leading to GLUT4 translocation, starting with activation of insulin receptors through signaling cascade involving phosphatidylinositol 3-kinase (PI3K) and protein kinase B (PKB) and finally, the action of their effectors. We will present regulatory mechanisms and modulators of insulin-mediated glucose uptake.","PeriodicalId":109929,"journal":{"name":"Blood Glucose Levels","volume":"2 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123422516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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