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Natural Products in the Treatment of Unremitting Wounds Secondary to Diabetes or Peripheral Vascular Disease
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
T1DM, previously known as juvenile dependent or insulin-dependent diabetes mellitus, accounts for 5–10% of people with diabetes. Traditionally diagnosed in children and teens, T1DM can occur in any age group. In T1DM, immunologic, genetic and environmental factors lead to a loss of beta cells within the pancreatic islets. The beta cells normally produce insulin, so when they are destroyed, there is a decrease in insulin production. Insulin normally functions to lower blood glucose, so the destruction of beta cells leads to hyperglycemia within the bloodstream. This prolonged state of hyperglycemia leads to the damage of other organs and vessels. Genetic factors, viral infections and toxins have all been found to be triggers for the loss of insulin production from pancreatic beta cells (Lucier and Weinstock, 2021).
Endocrine Disorders, Contraception, and Hormone Therapy during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Insulin is a hormone secreted by pancreatic beta cells that regulates glucose metabolism and other metabolic processes. Human insulin does not cross the placenta in physiologically significant amounts, but non-human insulin does. Subcutaneous injection is the usual route of administration for insulin, but in an emergency or during a stressful situation where a high degree of control is needed (e.g., labor, surgery), intravenous insulin is used to rapidly lower blood glucose.
Pathophysiology of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The pathogenesis of type 2 diabetes is not fully understood due to its complexity. Once insulin secretion cannot compensate for insulin resistance, hyperglycemia develops. Though insulin resistance is characteristic, beta cell dysfunction and impaired insulin secretion are common. There is impaired initial-phase insulin secretion as a response to IV glucose infusion, low pulsatile insulin secretion, and increased proinsulin secretion signaling impaired processing of insulin. There is also an accumulation of islet amyloid polypeptide, which is a protein usually secreted with insulin. Hyperglycemia may reduce insulin secretion because high glucose levels desensitize the beta cells. This causes glucose toxicity with beta cell dysfunction, or both. Usually, years pass as these changes to occur along with insulin resistance.
GABA treatment does not induce neogenesis of new endocrine cells from pancreatic ductal cells
Published in Islets, 2023
Shihao Wang, Xin Dong, Mahan Maazi, Nan Chen, Amarpreet Mahil, Janel L. Kopp
Pancreatic beta cells are lost through autoimmune-mediated destruction during the development of Type I diabetes. Efforts to replace these lost cells by potentially generating new beta cells from a source of endogenous cells have focused on increasing replication of existing beta cells or identifying potential non-beta cell sources, such as alpha, delta, acinar, or ductal cells.1–12 A promising method of generating new beta cells by inducing alpha cells to transdifferentiate into beta cells via transgenic Pax4 expression was suggested to be accompanied by generation of new alpha cells from ductal cells.1,3 Subsequently, it was discovered that gamma-aminobutyric acid (GABA) signaling could also increase beta cells and decrease alpha cells in mouse models and human islets1 and this raised the exciting possibility that it might be possible to increase beta cell numbers in patients using this method. In fact, a clinical trial was registered in 2018 to test the effects of long-term GABA administration in persons living with Type I diabetes, an indication of the excitement in the field at the potential of this molecule.
Myricetin derivative-rich fraction from Syzygium malaccense prevents high-fat diet-induced obesity, glucose intolerance and oxidative stress in C57BL/6J mice
Published in Archives of Physiology and Biochemistry, 2023
Devi Nallappan, Kien Chai Ong, Uma Devi Palanisamy, Kek Heng Chua, Umah Rani Kuppusamy
Obesity is a critical global health concern and the preponderance of obesity has been increasing in almost all nations. The number of obese and overweight individuals is expected to be more than half of the world’s population by 2030 (Tremmel et al. 2017). Obesity reflects a condition of an excess amount of body fat due to an imbalance between energy intake and energy expenditure (Jung and Choi 2014). The prolonged condition of obesity could lead to the development of numerous non-communicable diseases which include Type 2 Diabetes mellitus (T2DM) (Zheng et al. 2018). T2DM is a condition of hyperglycaemia resulting from high insulin resistance that occurs when insulin-responsive cells do not respond well to alleviate blood glucose levels. Over time, high insulin production damages beta cells of the pancreas and eventually results in beta cell failure (Yaribeygi et al. 2019). Emerging evidence suggested that obesity and T2DM are strongly associated with oxidative stress that results from elevated reactive oxygen species (ROS) levels in the body. In obesity, high level of ROS produced by hypertrophied adipocytes triggers damage to lipids, proteins and DNA, which leads to oxidative stress (Furukawa et al. 2004). This further leads to the systemic low-grade inflammation and finally the onset of metabolic syndrome and its complications (Biswas 2016).
The Relationship between the Lipid Accumulation Product and Beta-cell Function in Korean Adults with or without Type 2 Diabetes Mellitus: The 2015 Korea National Health and Nutrition Examination Survey
Published in Endocrine Research, 2022
Hye Eun Cho, Seung Bum Yang, Mi Young Gi, Ju Ae Cha, so Young Park, Hyun Yoon
Insulin resistance and beta cell dysfunction contribute to the development of T2DM.34 Pancreatic beta cells are the secretory cells that release insulin, an essential hormone regulating lipid and glucose metabolism. Excessive lipid accumulation causes detrimental effects on non-adipose tissues, such as skeletal muscle, liver, heart, kidney, and pancreatic beta cells.26,35 Lipotoxicity due to excessive lipid accumulation can contribute to beta-cell dysfunction and death by the generation of intracellular cytotoxic metabolites, such as free fatty acids, oxidative stress, glucolipotoxicity, and endoplasmic reticulum stress.36–38 In the context of lipid accumulation and beta-cell function, free fatty acids acutely increase glucose-stimulated insulin secretion through cell surface receptors and intracellular pathways.39 However, chronic exposure to free fatty acids, combined with elevated glucose (glucolipotoxicity), can impair the function and viability of beta cells.40