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Mahvash Disease
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Glucagon is a counterregulatory hormone for insulin, which lowers the extracellular glucose (usually stored in the liver as a polymer of glucose molecules or polysaccharide glycogen), and works to raise the concentration of glucose in the bloodstream through its binding to the glucagon receptor (GCGR, a G protein-coupled receptor of 485 aa) located in the plasma membranes of the liver (hepatocytes or liver cells) as well as the kidney, pancreas, heart, brain, and smooth muscle. This activates the stimulatory G protein, and then adenylate cyclase, triggering cAMP production and converting stored polysaccharide glycogen into glucose (i.e., glycogenolysis). After exhaustion of stored glycogen, glucagon promotes synthesis of additional glucose (i.e., gluconeogenesis) in the liver and kidneys. In addition, glucagon may shut off glycolysis in the liver, turning glycolytic intermediates into gluconeogenesis.
The Endocrine Pancreas
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Epinephrine is the other counterregulatory hormone of key importance. The contribution of adrenal activation toward correction of hypoglycemia increases with the severity of the stimulus. It turns out that the plasma glucose nadir rather than the change in level or even the rate of change is the major determinant of the peak epinephrine response.37 Physiologic increases in epinephrine that occur in response to hypoglycemia lead to both sustained increases in hepatic glucose production and suppression of peripheral glucose utilization.39 These mechanisms are mediated through both a- and p-adrenergic receptors. In addition, mobilization of certain fatty acids has been found to be an indirect effect of elevated epinephrine levels, and these fatty acids further enhance glucose production while limiting utilization.38 Although epinephrine deficiency (as would be seen after bilateral adrenalectomy or experimentally caused by both α and β blockade) does not impair glucose recovery from hypoglycemia if glucagon secretion is normal, the absence of both inevitably leads to severe hypoglycemia.
Shy-Drager Syndrome and Multiple System Atrophy
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Catecholamines affect intermediary metabolism through a variety of mechanisms. The importance of adrenaline as an hypoglycemic counter-regulatory hormone is highlighted by the fact that increases in plasma precede release of glucagon, growth hormone and Cortisol during hypoglycemia (Garber et al., 1976).
Incidence of diabetic ketoacidosis does not differ in Ramadan compared to other months and seasons: results from a 6-year multicenter study
Published in Current Medical Research and Opinion, 2023
Fateen Ata, Adeel Ahmad Khan, Ibrahim Khamees, Mohammed Bashir
The pathophysiology of diabetic ketoacidosis (DKA) is complex and involves multiple metabolic and hormonal changes1. The primary driver for DKA is insulin deficiency, either absolute (such as in T1D or advanced T2D with beta-cell dysfunction) or relative (such as in T2D or under-treated T1D)2. Insulin deficiency, coupled with the body’s inability to utilize glucose, results in multifactorial and unrestricted hyperglycemia2. Besides, the lack of insulin results in the loss of the storage of free fatty acids in the adipose tissue, resulting in excess free fatty acids, which are then converted into ketones by the liver2. The lack of insulin also triggers an uprise in the counter-regulatory hormones, such as cortisol, glucagon, epinephrine, norepinephrine, and growth hormone which further propagate hyperglycemia and ketonemia1.
Wheel running leads to sex-specific effects on Western diet-associated glucose homeostasis and brain insulin signaling without altering food-related impulsive choice
Published in Nutritional Neuroscience, 2022
Tiffany Y. Yang, Chan Young Choi, Francis A. Walter, Christopher S. Freet, Nu-Chu Liang
The metabolic results from OGTT and ITT from each sex were analyzed separately. Plasma glucose and insulin concentrations and their area under curve (AUC) from OGTT and ITT were analyzed using a 2-way mixed model ANOVAs. The first 30 min of ITT involves glucose translocation and uptake into the muscle and adipose thereby decreasing blood glucose levels and is a measure of insulin sensitivity [19]. After the nadir of blood glucose, the counter-regulatory response to hypoglycemia involving the activation of the sympathetic nervous system and release of counter-regulatory hormones including epinephrine, corticosterone, and glucagon, becomes initiated to bring glucose levels back to baseline [19]. Thus, the blood glucose concentration at the 90 min timepoint was analyzed using a 2-way factorial ANOVA (sex x exercise) to assess the counter-regulatory response.
In-patient outcomes of patients with diabetic ketoacidosis and concurrent protein energy malnutrition: A national database study from 2016 to 2017
Published in Postgraduate Medicine, 2021
Asim Kichloo, Hafeez Shaka, Zain El-Amir, Farah Wani, Jagmeet Singh, Genaro Romario Velazquez, Ehizogie Edigin, Dushyant Dahiya
DKA is aknown metabolic derangement of DM. Its morality rate is estimated to be 6–10% [8]. It can be a consequence of type 1 or type 2 DM [9,10]. In type 1 DM, DKA occurs as a result of decreased serum insulin secondary to β-cell destruction and decreased functional β-cells [9]. Decreased serum insulin leads to increases in counterregulatory hormones like cortisol, glucagon, growth hormone, and epinephrine [9]. This leads to increased hepatic gluconeogenesis and glycogenolysis increasing serum glucose concentrations [9]. Additionally, there is also decreased peripheral glucose uptake secondary to decreased insulin in the circulation, resulting in hyperglycemia and increased serum osmolality. Muscle proteolysis also contributes to hyperglycemia, and these processes ultimately result in osmotic diuresis [9]. Fatty acid production also occurs and is promoted by the presence of catecholamines, which results in increased redox reactions including the β-oxidation of free fatty acids. This results in ketone production [9]. Pyruvate depletion secondary to gluconeogenesis shifts fatty acids toward ketone production and away from the citric acid cycle, also resulting in excessive ketone production and ultimately ketoacidosis [9].