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Готові списки джерел за темами / Cardioautonomic function, beta cell insulin secretion, type 2 diabetes

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Добірка наукової літератури з теми "Cardioautonomic function, beta cell insulin secretion, type 2 diabetes"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Cardioautonomic function, beta cell insulin secretion, type 2 diabetes"

1

Khin, Phyu Phyu, Jong Han Lee, and Hee-Sook Jun. "Pancreatic Beta-cell Dysfunction in Type 2 Diabetes." European Journal of Inflammation 21 (January 30, 2023): 1721727X2311541. http://dx.doi.org/10.1177/1721727x231154152.

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Анотація:

Pancreatic β-cells produce and secrete insulin to maintain blood glucose levels within a narrow range. Defects in the function and mass of β-cells play a significant role in the development and progression of diabetes. Increased β-cell deficiency and β-cell apoptosis are observed in the pancreatic islets of patients with type 2 diabetes. At an early stage, β-cells adapt to insulin resistance, and their insulin secretion increases, but they eventually become exhausted, and the β-cell mass decreases. Various causal factors, such as high glucose, free fatty acids, inflammatory cytokines, and isle

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2

Masoodi, Shariq Rashid. "Decline in Beta-Cell Function among Adolescents with Type 2 Diabetes Mellitus." JMS SKIMS 20, no. 2 (2017): 115–16. http://dx.doi.org/10.33883/jms.v20i2.211.

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It is well known that beta-cell function declines over time in adults with type 2 diabetes mellitus (T2DM). The beta-cell dysfunction, initially characterized by impairment in the first phase of insulin secretion following glucose stimulation, advances to a decline in second phase insulin secretion as the disease progresses. But whether this decline in beta-cell function occurs in adolescents with T2DM is uncertain. Investigators prospectively compared beta-cell functioning over time between 39 adolescents with newly diagnosed T2DM (mean age, 15 years; body-mass index z-score, 2.4) and 32 obes

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3

Yan, Li-hui, Biao Mu, Da Pan, et al. "Association between small intestinal bacterial overgrowth and beta-cell function of type 2 diabetes." Journal of International Medical Research 48, no. 7 (2020): 030006052093786. http://dx.doi.org/10.1177/0300060520937866.

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Aims Previous studies suggest that small intestinal bacterial overgrowth (SIBO) is associated with type 2 diabetes. However, few studies have evaluated the association between SIBO and beta-cell function in type 2 diabetes. The aim of this study was to evaluate whether beta-cell function was associated with SIBO. Materials and methods One hundred four patients with type 2 diabetes were included in this study. Based on the presence of SIBO, the patients were divided into SIBO-positive and SIBO-negative groups. Oral glucose tolerance tests were performed. Insulin sensitivity was measured using 1

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4

Popovic, Ljiljana, Miroslava Zamaklar, Katarina Lalic, and Olga Vasovic. "Analysis of the effect of diabetes type 2 duration on beta cell secretory function and insulin resistance." Srpski arhiv za celokupno lekarstvo 134, no. 5-6 (2006): 219–23. http://dx.doi.org/10.2298/sarh0606219p.

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Diabetes type 2 is a chronic metabolic disorder. Pathogenesis of diabetes type 2 results from the impaired insulin secretion, impaired insulin action and increased endogenous glucose production. Diabetes evolves through several phases characterized by qualitative and quantitative changes of beta cell secretory function. The aim of our study was to analyze the impact of diabetes duration on beta cell secretory function and insulin resistance. The results indicated significant negative correlation of diabetes duration and fasting insulinemia, as well as beta cell secretory function assessed by H

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5

Konenkov, Vladimir Iosifovich, Vadim Valerievich Klimontov, Svetlana Viktorovna Michurina, M. A. Prudnikova, and I. Ju Ishenko. "Melatonin and diabetes: from pathophysiology to the treatment perspectives." Diabetes mellitus 16, no. 2 (2013): 11–16. http://dx.doi.org/10.14341/2072-0351-3751.

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Pineal hormone melatonin synchronizes insulin secretion and glucose homeostasis with solar periods. Misalliance between melatonin-mediated circadian rhythms and insulin secretion characterizes diabetes mellitus type 1 (T1DM) and type 2 (T2DM). Insulin deficiency in T1DM is accompanied by increased melatonin production. Conversely, T2DM is characterized by diminished melatonin secretion. In genome-wide association studies the variants of melatonin receptor MT2 gene (rs1387153 and rs10830963) were associated with fasting glucose, beta-cell function and T2DM. In experimental models of diabetes me

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6

Shvarts, V. "Inflammation of adipose tissue. Part 2. Pathogenetic role in type 2 diabetes mellitus." Problems of Endocrinology 55, no. 5 (2009): 43–48. http://dx.doi.org/10.14341/probl200955543-48.

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This review deals with the role of adipose tissue inflammation (ATI) in the development of type 2 diabetes mellitus (DM2). ATI is regarded as a link between obesity and DM2. The review illustrates the involvement of main adipokines in pathogenesis of DM2 and provides a detailed description of such factors as impaired adiponectin and stimulation of cytokine production responsible for metabolic disorders, activation of lipolysis, in adipocytes, increased fatty acid and triglyceride levels, suppression of insulin activity at the receptor and intracellular levels. Adipokines, in the first place cy

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7

Makaji, Emilija, Sandeep Raha, Michael G. Wade, and Alison C. Holloway. "Effect of Environmental Contaminants on Beta Cell Function." International Journal of Toxicology 30, no. 4 (2011): 410–18. http://dx.doi.org/10.1177/1091581811405544.

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There is an increasing concern that chemicals in the environment are contributing to the global rise in the prevalence of type 2 diabetes (T2D). However, there is limited evidence for direct effects of these chemicals on beta cell function. Therefore, the goals of this study were (1) to test the hypothesis that environmental contaminants can directly affect beta cell function and (2) examine mechanistic pathways by which these contaminants could affect beta cell function. Using mouse beta TC-6 cells, we examined the acute effects of 6 substances (benzo[a]pyrene, bisphenol A [BPA], propylparabe

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8

Tarlton, Jamie M. R., Steven Patterson, and Annette Graham. "MicroRNA Sequences Modulated by Beta Cell Lipid Metabolism: Implications for Type 2 Diabetes Mellitus." Biology 10, no. 6 (2021): 534. http://dx.doi.org/10.3390/biology10060534.

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Alterations in lipid metabolism within beta cells and islets contributes to dysfunction and apoptosis of beta cells, leading to loss of insulin secretion and the onset of type 2 diabetes. Over the last decade, there has been an explosion of interest in understanding the landscape of gene expression which influences beta cell function, including the importance of small non-coding microRNA sequences in this context. This review sought to identify the microRNA sequences regulated by metabolic challenges in beta cells and islets, their targets, highlight their function and assess their possible re

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9

Kim, Yong Kyung, Lori Sussel, and Howard W. Davidson. "Inherent Beta Cell Dysfunction Contributes to Autoimmune Susceptibility." Biomolecules 11, no. 4 (2021): 512. http://dx.doi.org/10.3390/biom11040512.

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Анотація:

The pancreatic beta cell is a highly specialized cell type whose primary function is to secrete insulin in response to nutrients to maintain glucose homeostasis in the body. As such, the beta cell has developed unique metabolic characteristics to achieve functionality; in healthy beta cells, the majority of glucose-derived carbons are oxidized and enter the mitochondria in the form of pyruvate. The pyruvate is subsequently metabolized to induce mitochondrial ATP and trigger the downstream insulin secretion response. Thus, in beta cells, mitochondria play a pivotal role in regulating glucose st

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10

Grubelnik, Vladimir, Jan Zmazek, Rene Markovič, Marko Gosak, and Marko Marhl. "Mitochondrial Dysfunction in Pancreatic Alpha and Beta Cells Associated with Type 2 Diabetes Mellitus." Life 10, no. 12 (2020): 348. http://dx.doi.org/10.3390/life10120348.

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Type 2 diabetes mellitus is a complex multifactorial disease of epidemic proportions. It involves genetic and lifestyle factors that lead to dysregulations in hormone secretion and metabolic homeostasis. Accumulating evidence indicates that altered mitochondrial structure, function, and particularly bioenergetics of cells in different tissues have a central role in the pathogenesis of type 2 diabetes mellitus. In the present study, we explore how mitochondrial dysfunction impairs the coupling between metabolism and exocytosis in the pancreatic alpha and beta cells. We demonstrate that reduced

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