Control of Blood Glucose Concentration

10 Key excerpts on "Control of Blood Glucose Concentration"

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  Clinical Chemistry

  • David White, Nigel Lawson, Paul Masters, Daniel McLaughlin(Authors)
  • 2016(Publication Date)
  • Garland Science

    (Publisher)

  CHAPTER

  2

  GLUCOSE

  IN THIS CHAPTER HORMONAL REGULATION OF BLOOD GLUCOSE CONCENTRATION GLUCOSE STORAGE AND METABOLISM INSULIN GLUCAGON MAINTENANCE OF GLUCOSE HOMEOSTASIS IN THE FED AND FASTING STATES GLYCATION OF PROTEINS HYPERGLYCEMIA AND DIABETES MELLITUS CLINICAL CHEMISTRY MARKERS OF GLYCEMIC CONTROL HYPOGLYCEMIA METABOLISM OF FRUCTOSE AND GALACTOSE INBORN ERRORS OF CARBOHYDRATE METABOLISM

  Glucose is the single common substrate that can be used by all tissues as an energy source. Although most tissues can also use fatty acids for energy, nervous tissue, red cells (erythrocytes), kidney, and, in normal circumstances, brain have an obligatory requirement for glucose (Table 2.1 ). It is for this reason that the maintenance of plasma glucose within a narrow concentration range (Table 2.2 ) is fundamental to health. The normal distribution range of blood glucose in the UK population is 4.1–5.9 mmol/L (74–106 mg/dL) with a slightly higher range for adults of 60 years and above of 4.4–6.4 mmol/L (80–115 mg/dL). Pathological consequences ensue when the glucose concentration lies outside of this range for prolonged periods; hypoglycemia is characterized by impaired mental function and severe hypoglycemia by coma, while hyperglycemia, particularly chronic hyperglycemia, promotes the insidious pathology of diabetes mellitus.

  TABLE 2.1 Major fuel sources consumed by tissues after a meal

  TABLE 2.2 Normal ranges for glucose, HbA1c, and associated parameters

  2.1 HORMONAL REGULATION OF BLOOD GLUCOSE CONCENTRATION

  Blood glucose concentration is maintained within the normal range (homeostasis) by the opposing actions of anabolic hormones, mainly insulin, which promote the removal of glucose from the circulation, and catabolic hormones, mainly glucagon and, in times of stress, also epinephrine, growth hormone, and cortisol, which promote the input of glucose into blood. For the most part, glucose homeostasis can be thought of as a balance between the actions of insulin and glucagon (insulin–glucagon ratio; Table 2.3

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  Endogenous and Exogenous Regulation and Control of Physiological Systems

  • Robert B. Northrop(Author)
  • 2020(Publication Date)
  • CRC Press

    (Publisher)

  7    Regulation of Blood Glucose 7.0    INTRODUCTION In this chapter, the regulation of blood glucose in normal humans will be described and mathematically modeled. The roles of the pancreatic hormones insulin and glucagon in maintaining normoglycemia will be described, and the sources and sinks of glucose in the body, including storage in the liver as glycogen, will be examined. Dynamics will be stressed wherever possible. Next, the condition type I diabetes mellitus and insulin therapy will be considered and modeled. Finally, the designs of various “artificial beta cells” that attempt to regulate blood glucose by monitoring its concentration and computing an exogenous insulin infusion rate will be reviewed. The reason glucose is important in the body is that it is the principal source of energy for cell metabolism. There are a number of biochemical pathways whereby other sugars, starches, fats, and proteins in the diet can be converted to glucose. Once in the circulatory system, there are many sinks for glucose: 1.  It is stored in the liver, and to a lesser degree in muscle cells, as a high-molecular-weight polymer, glycogen. 2.  It can be lost in the urine if the blood glucose concentration rises above a threshold (about 1.8 g/l). 3.  It diffuses into insulin-sensitive cells (such as muscle cells) at a rate determined by the concentration gradient of glucose across the cell membranes. This gradient is the glucose concentration difference between extracellular (EF) and intracellular fluid (IF). If a person is exercising, muscle cells metabolize glucose at an increased rate. The diffusion constant for glucose on insulin-sensitive cells increases monotonically with the concentration of insulin

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  Vital Signs for Nurses

  An Introduction to Clinical Observations

  • Joyce Smith, Rachel Roberts(Authors)
  • 2011(Publication Date)
  • Wiley-Blackwell

    (Publisher)

  Chapter 11 Blood Glucose Monitoring Introduction Blood glucose monitoring is an important part of the patient's vital signs and is central to the assessment process. Glucose is required by the body to maintain the body's metabolism, and any deviation from the normal range may result in an altered level of consciousness in the patient. Obtaining a sample of blood from the patient is the first step towards measuring the glucose levels within the body. Learning Outcomes By the end of this chapter, you will be able to discuss the following: The anatomy and physiology related to blood glucose Stress response Abnormal/normal blood glucose readings Diabetes How to perform equipments checks/quality control test How to obtain a capillary blood sample Cleaning and storage of the glucose monitor Documentation Policies and guidelines Anatomy and Physiology The two major glands within our body that are involved in maintaining blood glucose levels are the liver and the pancreas. The liver is the largest gland in the body and the portal vein enters the liver, carrying blood from the stomach and pancreas. The pancreas is a pale grey gland that is about 12–15 cm long and lies behind the stomach (Waugh and Grant, 2006). Within the gland are specialised cells that are called the Islets of Langerhans that produce the hormones insulin and glucagon. The beta cells secrete insulin to promote carbohydrate metabolism and the alpha cells secrete glucagon that stimulates glycogenolysis in the liver (Watkins et al., 2003). Both hormones are stimulated by fluctuating blood glucose levels that flow directly into the blood stream. These two hormones work together to regulate blood glucose levels, ensuring that they are maintained within the normal range of 4–7 mmol/l (Ferguson, 2005). For our brain to function effectively, it needs both oxygen and glucose

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  Blood Glucose Levels

  • Leszek Szablewski(Author)
  • 2020(Publication Date)
  • IntechOpen

    (Publisher)

  Section 2 Regulation of Glucose Levels 9 Chapter 2 Molecular Basis of Blood Glucose Regulation Asma Ahmed and Noman Khalique 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 pan-creatic 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 pro-duction 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. Keywords: genes, molecular and cellular targets, hormones, pathways 1. Introduction Blood glucose is regulated by the pancreatic hormones alone or in combination with other endocrine glands and all this is controlled by one or more gene or cellular or molecular targets.

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  Current Topics in Cellular Regulation

  • Bernard L. Horecker, Earl R. Stadtman(Authors)
  • 2014(Publication Date)
  • Academic Press

    (Publisher)

  According to this con-cept, homeostasis of the glycemia is essentially achieved by an intrinsic hepatic mechanism, which responds by glucose uptake or release to a signal from the concentration of glucose in the blood flowing through the liver: the fundamental regulation of the blood sugar is an autoregulation, 51 52 W r ILLY STALMANS in which the prime mover is the blood sugar level itself (182). In the actual process that converts the liver function from glucose output to glucose uptake following food intake, he introduced a further distinction: in the normal animal, a rise in the blood sugar level causes the liver to respond by diminishing its output of sugar to the blood (181) ; this phenomenon Soskin called the hepatic inhibition of glucose release. And it was added, at that moment rather speculatively: it seems logical to assume that smaller amounts of sugar . . . may be fully compensated for by hepatic inhibition alone. Larger amounts of sugar will invoke hepatic storage as well (182). The critical blood glucose level (thresh-old) at which the liver function switches between glucose output and uptake in a particular animal depends largely upon the endocrine bal-ance, and coincides with the level of blood sugar which that animal habitually maintains (181). It should be noted that the role of insulin in the endocrine balance was duly stressed. It is feasible, of course, to consider the glucostatic function of the liver as being solely governed by the command of hormonal substances (e.g., insulin and glucagon), the secretion of which is in turn determined by the blood glucose level as well as by other factors. Such a theory, however, would fail to appreciate the intrinsic hepatic mechanism which, as will be shown, is now well established. Undoubtedly, the main values of Soskin's concept have been the recognition of the different basic principles that determine glucose homeostasis by the liver, and the assignment of a proper place to each in a nonexclusive way.

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  Process Dynamics and Control

  • Dale E. Seborg, Thomas F. Edgar, Duncan A. Mellichamp, Francis J. Doyle, III(Authors)
  • 2016(Publication Date)
  • Wiley

    (Publisher)

  In the medical field, as in the process domain, there are three essen- tial requirements for implementing feedback control: (1) the availability of a measurement that indicates the condition of the patient, (2) some knowledge of the underlying process dynamics (e.g., the effect of a drug on a patient’s response), and (3) a suitable manip- ulated variable (e.g., drug or medication). Since 1990, there have been dramatic advances in sensor technol- ogy, as well as modeling and control strategies, for a variety of medical problems (see, for example, Morari and Gentilini, 2001; Hahn et al., 2002; Heller, 2005; Doyle et al., 2007; Carson and Cobelli, 2013; Hacısalihzade, 2013). In the following sections, a diverse range of biomedi- cal applications that motivate the application of process control are described. 23.2.1 Type 1 Diabetes In a healthy individual, the concentration of blood sugar (glucose), the body’s primary energy source, is regu- lated primarily by the pancreas, using a combination of manipulated inputs that are analogous to the brake and gas pedal system used to control the speed of an auto- mobile. As the blood sugar falls, the pancreas responds with the release of the hormone glucagon from the α-cells, which stimulates the breakdown of glycogen in the liver to create glucose, thus leading to an increase in glucose (i.e., the gas pedal). On the other hand, as blood glucose rises, the pancreatic β-cells release the hormone insulin that stimulates the uptake of glucose by muscle and fat tissue (Carson and Cobelli, 2013), and, consequently, the blood glucose level is decreased (i.e., the brake). Type 1 diabetes mellitus is a disease characterized by failure of the pancreatic β-cells. In contrast, the primary manifestation of Type 2 diabetes is an inability, or resistance, of the cells to respond to insulin. The only treatment for Type 1 diabetes consists of exoge- nous insulin injections, traditionally administered in an open-loop manner by the patient.

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  Textbook of Diabetes

  • Richard I. G. Holt, Allan Flyvbjerg(Authors)
  • 2024(Publication Date)
  • Wiley-Blackwell

    (Publisher)

  Central Control of Glucose Homeostasis Chapter 10 139 References 1 Bernard, C. (1849). C. R. Soc. Bio. 1: 60. 2 Oh, Y., Lai, J.S.-Y., Mills, H.J. et al. (2019). Nature 574: 559–564. 3 D’Alessio, D.A., Kieffer, T.J., Taborsky, G.J. Jr., and Havel, P.J. (2001). J. Clin. Endocrinol. Metab. 86: 1253–1259. 4 Carey, M., Lontchi-Yimagou, E., Mitchell, W. et al. (2020). Diabetes 69 (6): 1140–1148. 5 Woods, S.C. and Porte, D. Jr. (1974). Physiol. Rev. 54: 596–619. 6 Osundiji, M.A. and Evans, M.L. (2013). Endocrinol. Metab. Clin. N. Am. 42: 1–14. 7 Tang, S.C., Baeyens, L., Shen, C.-N. et al. (2018). Diabetologia 61: 168–181. 8 Havel, P.J., Veith, R.C., Dunning, B.E., and Taborsky, G.J. Jr. (1988). J. Clin. Invest. 82: 1538–1545. 9 Perseghin, G., Regalia, E., Battezzati, A. et al. (1997). J. Clin. Invest. 100: 931–941. 10 Teff, K.L. (2011). Physiol. Behav. 103: 44–50. 11 Thorens, B. (2014). Diabetes Obes. Metab. 16 (Suppl 1): 87–95. 12 Jessen, L., Smith, E.P., Ulrich-Lai, Y. et al. (2017). Endocrinology 158 (7): 2124–2133. 13 Capozzi, M.E., Svendsen, B., Encisco, S.E. et al. (2019). JCI Insight 4 (5): e126742. 14 Rosario, W., Singh, I., Wautlet, A. et al. (2016). Diabetes 65 (9): 2711–2723. 15 Jansen, A.S., Hoffman, J.L., and Loewy, A.D. (1997). Brain Res. 766: 29–38. 16 Buijs, R.M., Chun, S.J., Niijima, A. et al. (2001). J. Comp. Neurol. 431: 405–423. 17 Tokunaga, K., Fukushima, M., Kemnitz, J.W., and Bray, G.A. (1986). Endocrinology 119: 1708–1711. 18 Coomans, C.P., van den Berg, S.A.A., Lucassen, E.A. et al. (2013). Diabetes 62: 1102–1108. 19 Rui, L. (2014). Compr. Physiol. 4: 177–197. 20 Ding, G., Li, X., Hou, X. et al. (2021). Nature 592: 763–767. 21 Meek, T.H., Nelson, J.T., Matsen, M.E. et al. (2016). Proc. Natl. Acad. Sci. U. S. A. 113: E2073–E2082. 22 Burdakov, D. and González, J.A. (2009). Acta Physiol. (Oxf.) 195: 71–78. 23 Shimazu, T. and Minokoshi, Y. (2017). J. Endocr. Soc. 1: 449–459. 24 Hirschberg, P.R., Sarkar, P., Teegala, S.B., and Routh, V.H.

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  Handbook of Optical Sensing of Glucose in Biological Fluids and Tissues

  • Valery V. Tuchin(Author)
  • 2008(Publication Date)
  • CRC Press

    (Publisher)

  8 Handbook of Optical Sensing of Glucose FIGURE 1.5: Simplified scheme of blood glucose level regulation. Comments are in the text. 1.2.3 Regulation of glucose metabolism: main pathways and processes Regulation of glucose metabolism is still in the area of uncertainty. One of the accepted hypotheses still of current importance is the food and famine hypothe-sis, which considers effects of meals and periods between them on blood glucose concentration and glucose uptake and output [19]. The hypothesis deals with three time periods: prandial and immediate postprandial, delayed postprandial, and re-mote postprandial periods. During these periods the reciprocal relations between glucoregulatory hormones have taken place. Glucoregulatory hormones include insulin, glucagon, amylin, GLP-1, glucose-dependent insulinotropic peptide (GIP), epinephrine, cortisol, and growth hormone. Of these, insulin and amylin are derived from the β -cells, glucagon from the α -cells of the pancreas, and GLP-1 and GIP from the L-cells of the intestine (Fig. 1.5). Amylin is a neuroendocrine hormone expressed and secreted with insulin as a re-sponse to nutrient stimuli [20–23]. In healthy adults, fasting plasma amylin concen-trations range from 4 to 8 pmol/l rising as high as 25 pmol/l postprandially. In dia-betic patients, amylin is deficient (IDDM) or impaired (NIDDM) [24, 25]. Amylin’s main task is to prevent an abnormal rise in glucose concentrations via two main mechanisms: suppression of postprandial glucagon secretion [26], and inhibition of the rate of gastric emptying [27]. GIP stimulates insulin secretion and regulates fat metabolism, but does not inhibit glucagon secretion or gastric emptying [28]. GLP-1 stimulates insulin secretion in the pancreas [29, 30]. Artificial infusion of GLP-1 results in decrease of postprandial glucose as well as fasting blood glucose concentrations. GLP-1 helps to regulate

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  Forensic Aspects of Hypoglycaemia

  First Edition

  • Vincent Marks(Author)
  • 2019(Publication Date)
  • CRC Press

    (Publisher)

  1 The Control of Blood Glucose in Health and Disease: Hypoglycaemia

  Introduction

  No one definition of hypoglycaemia satisfies all situations; context is important. Literally, hypoglycaemia means ‘abnormally low blood glucose concentration’; in other words, it is a numerical value below an arbitrarily defined ‘normal’ or reference value. It may be completely asymptomatic.

  Medically, hypoglycaemia is a physical sign (consequence) of disease and is, itself, able to cause characteristic signs and symptoms. These are described as a hypoglycaemic attack and by patients on antidiabetic therapy as a ‘hypo’. In them, a ‘hypo’ is a characteristic set of symptoms regardless of whether their blood glucose concentration is demonstrably low or not.

  To the clinical scientist, hypoglycaemia is the blood glucose concentration below which certain well-defined physiological reactions occur which may, or may not, be accompanied by subjective symptoms.

  To the clinical biochemist, hypoglycaemia is the level of blood glucose below the 95% confidence limits for the normal, healthy population: with an intermediate zone of uncertainty.

  Most clinicians distinguish between hypoglycaemia arising in diabetic people due to treatment (iatrogenic) and those who are not diabetic (spontaneous). For most clinical purposes, a blood glucose concentration below 2.5 mmol/L in people under the age of 60, and below 3.0 mmol/L in older people, must be treated as hypoglycaemia worthy of investigation.

  Hypoglycaemia is important in a forensic context because it can produce profound but ephemeral effects upon brain function that can cause the sufferer to behave in a bizarre and totally uncharacteristic way that brings them into conflict with the law. It can also lead to permanent brain damage or death.

  The typical signs and symptoms of hypoglycaemia are shown in Table 1.1

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  Chemically Modified Minds

  Substance Use for Cognitive Enhancement

  • Matthew Hall, Mark Forshaw, Catharine Montgomery, Matthew Hall, Mark Forshaw, Catharine Montgomery(Authors)
  • 2020(Publication Date)
  • Palgrave Macmillan

    (Publisher)

  It is feasible to exploit the glucose enhancement effects to enhance cognition short term, with the caveat that repeated hyperglycaemia would be detrimental longer term to glucoregulatory control, as evidenced by the implication of poor glycaemic control in cognitive decline. However, understanding the role of glucose and glycaemic control on cognition offers the intriguing possibility to exploit these mechanisms responsibly.

  Through understanding the impact of self-control in reducing blood glucose levels and subsequent self-control/willpower, we gain an insightful understanding of everyday behaviours. Knowing that a glucose load (or consumption of a calorific source to raise blood glucose) reinstates self-control hints at a powerful tool to moderate everyday behaviour, for example, in assisting individuals to make better food choices, ultimately enhancing health and mitigating risk factors associated with declining glucoregulatory disorders. Strict dieting requires continuous self-control and willpower, often to no avail, with overeating on calorie-dense food later in the day, effectively sabotaging any calorific deficit. This knowledge can allow us to develop more effective strategies to manage cognitive self-control and decision-making.

  Glucose is particularly effective in enhancing (or moderating deficits in) declarative memory, specifically during high cognitive demand. Often, we can anticipate situations in which we will encounter significant cognitive demand and declarative memory, for example job interviews, exams, public speaking, busy work periods. Effectively managing glucose levels within such situations can facilitate our performance.

  The effect of glucose is far from straight forwards, with many moderating factors. What we do know, is that suboptimal circulatory glucose levels are detrimental to cognitive functioning, even in healthy populations. So, while there is scope to utilise elevated glucose as a cognitive enhancer (short term), a more responsible approach is to effectively manage glucoregulatory control long term to mitigate risk factors associated with conditions presenting with cognitive impairments and cognitive decline.

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