Glucagon and Its Effects on Hypoglycemia Patients

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Glucagon and Its Effects on Hypoglycemia Patients

The organs that aggravate or alleviate hypoglycemia entail the pancreas, liver, and muscles. Each organ contains specific enzymes and hormones that participate in the metabolic process, regulating blood sugar and maintaining equilibrium (Melmed et al., 2020). Glucagon raises blood sugar levels and keeps them from falling too low, whereas insulin lowers blood sugar levels. Defects of insulin output by beta cells have been the main driver of diabetes, whose effects are counteracted by glucagon (Matfin, 2018). The pancreas contains two critical cells, the alpha and beta cells which work together to regulate blood sugar levels. The alpha cells produce glucagon while the beta cells produce insulin. The liver serves as the bodys glucose repository, thus facilitating the process of maintaining normal blood sugar levels (Hod et al., 2018). The liver cells are responsible for reserving glucose in glycogen molecules in a healthy patient and generate glycogen breakdown in the glycolysis mechanism when blood glucose is low.

Glucagon influences blood sugar levels through glycogenolysis and gluconeogenesis. In glycogenolysis, the alpha cells increase the production of glucagon, which stimulates the conversion of glycogen stored in the liver into glucose (Puri, 2020). The converted glucose is then released into the bloodstream, thus leading to increased blood sugar levels (Vasudevan, 2019). Glucagon stimulates gluconeogenesis, where the liver produces more glucose from amino acid molecules (Wewer Albrechtsen et al., 2019). The hormone prevents the increased use of glucose in muscle cells by reducing how much glucose the liver has, thus releasing the extra glucose into muscle cells (McConnell, 2020). Muscle cells use glucose for glycolysis, the pathway for producing energy, via a complex mechanism mediated by insulin. Glucagon receptors are not present in skeletal muscles, thus do not activate these cells to begin glycolysis, which uses glucose for ATP production, increasing glucose levels in the blood.

Pathophysiology

Glucagon affects the social life of patients with type-2 diabetes when produced at high levels. The alpha cells in type-2 diabetes become resistant to insulin, like liver, fat, and muscle cells. The result is that glucagon release is no longer inhibited during mealtime, leading to a rise in blood glucose and, consequently, the elevated hormone levels in type 2 diabetes (Jorgens & Porta, 2020). Further, glucagon-induced insulin resistance aggravates the insulin-deficient states metabolic consequences, accumulating glucose as glycogen in the liver and pancreatic tumors called glucagonomas (Ando et al., 2021).

These functional tumors accelerate glucagon production, leading to severe and life-threatening symptoms. Glucagonoma is a type of neuroendocrine tumor (NET) that starts in the pancreas, and its symptoms are vague as they develop slowly. The main symptoms of glucagonomas entail weight loss and deep vein thrombosis (Winter et al., 2020). Glucagonomas are malignant and thus spread into other organs and tissues, usually the liver interfering with its functions (Wewer Albrechtsen et al., 2019). High blood sugar can lead to renal rupture that precipitates sickle-cell anemia. The disease leads to vaso-occlusion, where the sick red blood cells block blood flow to other body parts, leading to an inflammatory response. When the blood forms solid clots, it causes pain in the patient.

Pharmacology

Glucagonomas are treated through surgery to remove the cancerous cells. The pharmacology in sickle-cell anemia depends on the severity of the pain caused by blood clots. Treatment should range from mild to strong doses depending on the patient pain level. Non-steroidal anti-inflammatory drugs (NSAIDs) such as diclofenac and ibuprofen are administered to patients with vaso-occlusion (Wewer Albrechtsen et al., 2019). Opioids are used when the pain persists, indicating the NSAIDs are inadequate. The most preferred opioids are morphine, levorphanol, methadone, oxymorphone, and fentanyl.

Reference

Ando, H., Ukena, K., & Nagata, S. (2021). Handbook of hormones: Comparative endocrinology for basic and clinical research. (2^nd ed.). Academic Press.

Connel, T. H. (2020). Study guide for the nature of disease. (2^nd ed.). Jones & Bartlett Learning.

Hod, M., Jovanovic, L. G., Renzo, G. C., Leiva, A., & Langer, O. (2018). Textbook of diabetes and pregnancy. (3^rd ed.). CRC Press.

Jorgens, V., & Porta, M. (2020). Unveiling diabetes historical milestones in diabetology. Karger Medical and Scientific Publishers.

Matfin, G. (2018). Endocrine and metabolic medical emergencies: A clinicians guide. (2^nd ed.). John Wiley & Sons.

Melmed, S., Koenig, R., Rosen, C., Auchus, R., & Goldfine, A. (2020). Williams textbook of endocrinology. (14^th ed.). Elsevier Health Sciences.

Puri, D. (2020). Textbook of medical biochemistry. (4^th ed.). Elsevier Health Sciences.

Vasudevan, D. M., Sreekurami, S., & Vaidyanathan, K. (2019). Textbook of biochemistry for medical students. Jaypee Brothers Medical Publishers.

Wewer Albrechtsen, N. J., Pedersen, J., Galsgaard, K. D., Winther-Sørensen, M., Suppli, M. P., Janah, L., Gromada, J., Vilstrup, H., Knop, F. K., & Holst, J. J. (2019). The Liver±-Cell Axis and Type 2 Diabetes. Endocrine Reviews, 40(5), 13531366. Web.

Winter, W. E., Sokoll, L., Holmquist, B., & Bertholf, R. L. (2020). Handbook of diagnostic endocrinology. (3^rd ed.). Academic Press.

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