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Hypothalamic Neuronal Circuits Are Modulated by Insulin and Impact Metabolism 1
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Tadeu de Oliveira Diz, Sabela Casado, Rubén Nogueiras, Sulay Tovar
Pancreatic β-cells secrete insulin into the circulation, and the principal regulator of insulin secretion is blood glucose. Post-meal spikes in blood glucose induce rapid insulin secretion into blood circulation that affects several organs, including the hypothalamus. The level of hypothalamic insulin depends on the amount of blood insulin transported in the brain and on insulin potentially originating from local sources.
Carrier Screening For Inherited Genetic Conditions
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Whitney Bender, Lorraine Dugoff
Clinical features: This syndrome is characterized by excessive insulin secretion. One-third of infants are macrosomic at delivery due to hyperinsulinemia in fetal life. Persistent hypoglycemia is often recognized within the first few days of life.
Diabetes
Published in Awanish Kumar, Ashwini Kumar, Diabetes, 2020
Our body utilises the glucose obtained from food immediately, or it is converted to glycogen and stored in the liver and muscles as storage polysaccharide or adipose triglyceride (energy reservoir). Insulin is the hormone which controls this action. Diabetes mellitus occurs when the body is no longer capable of taking the blood glucose inside cells and utilise the glucose for different cellular activities. T2DM occurs when the body is either not able to utilise the insulin produced (insulin resistance) or is not producing enough insulin (damage to β-cells due to glucotoxicity). A decreased insulin secretion results from impairment in glucose response by insulin secreting β-cells of the pancreas. A mutation in the glucokinase gene, which plays an important role in the glucose-sensing mechanism of pancreatic beta cells, is also an important factor of impaired glucose tolerance in the pancreas. Insulin resistance, on the other hand, is the condition when the insulin receptors become less responsive towards insulin even when the hormone is present in a physiological amount. This condition is attributed to many factors; the major factor being obesity, which exerts its effect via free fatty acids and inflammatory cytokines (such as TNF-α) which downregulate the insulin receptor and insulin receptor substrate (IRS) protein [4,5].
Impacts of the COVID-19 pandemic on a human research islet program
Published in Islets, 2022
Tina J. Dafoe, Theodore Dos Santos, Aliya F. Spigelman, James Lyon, Nancy Smith, Austin Bautista, Patrick E. MacDonald, Jocelyn E. Manning Fox
Although increased shipping times likely accounts for much of the increase in negative feedback, we wondered whether poorer islet outcomes and performance may be driving some decrease in the perception of islet quality. Insulin secretion in response to 1 mM, 10 mM and 16.7 mM glucose is measured for each prep as part of our standard quality assurance and human islet phenotyping program. The total islet insulin content (Figure 6(a)), and insulin secretory response to glucose, whether expressed as absolute values (Figure 6 (bi)), percent content (Figure 6(bii)) or stimulation index (Figure 6(biii)), was unchanged during the pandemic. Other in-house parameters of islet quality and function were similarly unchanged (Figure 7) including preparation purity, percentage of islets trapped in acinar, islet particle index, and insulin content per IEQ. The mean duration in culture prior to distribution and the percentage recovery following culture were also unchanged. Together, these findings suggest that the perceived reduction in the quality of islets reported by recipient groups was likely due to shipping disruptions and the ensuing extended duration that islets were subjected to suboptimal culture conditions during transit.33–36
Purine metabolites can indicate diabetes progression
Published in Archives of Physiology and Biochemistry, 2022
Yogaraje Gowda C. Varadaiah, Senthilkumar Sivanesan, Shivananda B. Nayak, Kashinath R. Thirumalarao
Numerous pathogenic processes are involved in the development of diabetes which includes autoimmune destruction of the pancreatic β-cells with consequent insulin shortage and abnormalities that result in resistance to insulin action. The origin of the abnormalities in carbohydrate, fat, and protein metabolism in diabetes is lack of insulin action on target tissues (Shaaban et al. 2016). Reduced insulin action results from insufficient insulin secretion and/or reduced tissue responses to insulin at one or additional points in the complex pathways of hormone action. Impairment of insulin secretion and defects in insulin action regularly exist in the same patient, and it is often unclear which abnormality, if either alone, is the primary reason of the hyperglycemia (American Diabetes Association 2013). Based on epidemiological studies, the prevalence of diabetes has increased worldwide, which has led to an increased burden on the people and healthcare systems (Oldroyd et al. 2005).
Neuroendocrine tumor with diarrhea: not always the usual suspects – a case report of metastatic calcitoninoma with literature review
Published in Acta Clinica Belgica, 2021
Kenny Vlaemynck, Marc De Man, Kathia De Man, Anne Hoorens, Karen Geboes
Among functioning PanNENs, immunohistochemical expression of calcitonin was almost exclusively found in insulinomas [1]. This suggests that both insulinomas and calcitoninomas are derived from the beta-cells of the islets of Langerhans. Insulin secretion from the pancreatic beta-cells is mainly regulated by glucose, entering the beta-cells via glucose transporters (GLUT). The presence of glucose transporters on the cell membrane could explain the FDG uptake established by 18FDG PET-CT scan despite the low proliferation rate. Although the exact mechanisms of action are not yet well defined, there also seems to be a role for serotonin in the control of insulin release from the beta-cells. Binding of serotonin on 5-HT3 receptors of the beta-cells stimulates insulin secretion [10]. As a result, stimulation of calcitonin release through serotonin binding can be suspected. We indeed assume that the very high calcitonin levels in our case are causing secretory diarrhea.