Excess Glucose Intake Induces Accelerated β-Cell Polyploidization in Normal Mice: A Possible Deleterious Effect

1985 ◽  
Vol 115 (2) ◽  
pp. 271-278 ◽  
Author(s):  
James W. White ◽  
Frank J. Swartz ◽  
Andrew F. Swartz
Keyword(s):  
Deleterious Effect ◽  
Β Cell ◽  
Glucose Intake ◽  
Excess Glucose

Longitudinal Glycaemic Profiles during Remission in 6q24-Related Transient Neonatal Diabetes Mellitus

2021 ◽  
Vol 94 (5-6) ◽  
pp. 229-234
Author(s):  
Yasuhiro Sato ◽  
Tsuyoshi Isojima ◽  
Kiyomi Takamiya ◽  
Kahoko Motoyama ◽  
Shigehiro Enkai ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cell Function ◽  
Neonatal Diabetes ◽  
Model Assessment ◽  
Homeostasis Model Assessment ◽  
Β Cell ◽  
Transient Neonatal Diabetes Mellitus ◽  
Glucose Intake ◽  
Β Cell Function ◽  
Transient Neonatal Diabetes

<b><i>Introduction:</i></b> Transient neonatal diabetes mellitus (TNDM) is a rare condition that is characterized by the presence of diabetes mellitus during the first 6 months of life and remission by 18 months of age. It usually relapses at a median age of 14 years. Hyperinsulinaemic hypoglycaemia is a relatively common complication during remission. Although β-cell function is reported to be impaired at relapse, the clinical course of glycaemic profiles during remission in patients with TNDM remains largely unknown. <b><i>Case Presentation:</i></b> Longitudinal glycaemic profiles were investigated annually from remission (185 days) to relapse (14.5 years) in a patient with TNDM due to paternal 6q24 duplication using the oral glucose tolerance test (glucose intake: 1.75 g/kg to a maximum of 75 g). The patient’s β-cell function and insulin sensitivity were assessed by calculating the insulinogenic index, homeostasis model assessment of β-cell function (HOMA-β), homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index, and Matsuda index. Early insulin response to glucose intake was impaired throughout remission, whereas fasting insulin and β-cell function by HOMA-β gradually increased in the first few years since remission, followed by a gradual decline in function. In contrast, HOMA-IR fluctuated and peaked at 6.5 years of age. <b><i>Conclusion:</i></b> This is the first report of annual longitudinal glycaemic profiles in a patient with 6q24-related TNDM during remission. We identified fluctuations in β-cell function and insulin resistance during remission.

scholarly journals Glutathione prevents chronic oscillating glucose intake-induced β-cell dedifferentiation and failure

2019 ◽  
Vol 10 (4) ◽  
Author(s):  
Jitai Zhang ◽  
Hui An ◽  
Kaidi Ni ◽  
Bin Chen ◽  
Hui Li ◽  
...  
Keyword(s):  
Β Cell ◽  
Cell Dedifferentiation ◽  
Glucose Intake ◽  
Oscillating Glucose

Ultrastructural investigation of an adenoma of the pituitary post mortem

1987 ◽  
Vol 45 ◽  
pp. 622-623
Author(s):  
Shirley Siew ◽  
W. C. deMendonca
Keyword(s):  
Deleterious Effect ◽  
Anterior Lobe ◽  
Definitive Diagnosis ◽  
Pars Intermedia ◽  
Post Mortem ◽  
Close Apposition ◽  
Autopsy Material ◽  
Progressive Loss ◽  
Transmission Electron ◽  
Means Of Transmission

The deleterious effect of post mortem degeneration results in a progressive loss of ultrastructural detail. This had led to reluctance (if not refusal) to examine autopsy material by means of transmission electron microscopy. Nevertheless, Johannesen has drawn attention to the fact that a sufficient amount of significant features may be preserved in order to enable the establishment of a definitive diagnosis, even on “graveyard” tissue.Routine histopathology of the autopsy organs of a woman of 78 showed the presence of a well circumscribed adenoma in the anterior lobe of the pituitary. The lesion came into close apposition to the pars intermedia. Its architecture was more compact and less vascular than that of the anterior lobe. However, there was some grouping of the cells in relation to blood vessels. The cells tended to be smaller, with a higher nucleocytoplasmic ratio. The cytoplasm showed a paucity of granules. In some of the cells, it was eosinophilic.

Adipokines as key players in β cell function and failure

2019 ◽  
Vol 133 (22) ◽  
pp. 2317-2327 ◽  
Author(s):  
Nicolás Gómez-Banoy ◽  
James C. Lo
Keyword(s):  
Metabolic Diseases ◽  
Cell Function ◽  
Whole Body ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Axis ◽  
Β Cell Function ◽  
Prevalence Of Obesity ◽  
Specific Factors ◽  
Whole Body Metabolism

Abstract The growing prevalence of obesity and its related metabolic diseases, mainly Type 2 diabetes (T2D), has increased the interest in adipose tissue (AT) and its role as a principal metabolic orchestrator. Two decades of research have now shown that ATs act as an endocrine organ, secreting soluble factors termed adipocytokines or adipokines. These adipokines play crucial roles in whole-body metabolism with different mechanisms of action largely dependent on the tissue or cell type they are acting on. The pancreatic β cell, a key regulator of glucose metabolism due to its ability to produce and secrete insulin, has been identified as a target for several adipokines. This review will focus on how adipokines affect pancreatic β cell function and their impact on pancreatic β cell survival in disease contexts such as diabetes. Initially, the “classic” adipokines will be discussed, followed by novel secreted adipocyte-specific factors that show therapeutic promise in regulating the adipose–pancreatic β cell axis.

Cognitive Load Mediates the Effect of Emotion on Analytical Thinking

2016 ◽  
Vol 63 (6) ◽  
pp. 343-350 ◽  
Author(s):  
Bastien Trémolière ◽  
Marie-Ève Gagnon ◽  
Isabelle Blanchette
Keyword(s):  
Cognitive Load ◽  
Secondary Task ◽  
Deleterious Effect ◽  
Detrimental Effect ◽  
Emotional Problems ◽  
Syllogistic Reasoning ◽  
Cognitive Resources ◽  
Potential Explanation ◽  
Cognitive Mechanism ◽  
Analytical Thinking

Abstract. Although the detrimental effect of emotion on reasoning has been evidenced many times, the cognitive mechanism underlying this effect remains unclear. In the present paper, we explore the cognitive load hypothesis as a potential explanation. In an experiment, participants solved syllogistic reasoning problems with either neutral or emotional contents. Participants were also presented with a secondary task, for which the difficult version requires the mobilization of cognitive resources to be correctly solved. Participants performed overall worse and took longer on emotional problems than on neutral problems. Performance on the secondary task, in the difficult version, was poorer when participants were reasoning about emotional, compared to neutral contents, consistent with the idea that processing emotion requires more cognitive resources. Taken together, the findings afford evidence that the deleterious effect of emotion on reasoning is mediated by cognitive load.

Lactate overrides central nervous but not β-cell glucose sensing in humans

2008 ◽  
Vol 116 (09) ◽  
Author(s):  
SM Schmid ◽  
M Hallschmid ◽  
K Jauch-Chara ◽  
KM Oltmanns ◽  
A Peters ◽  
...  
Keyword(s):  
Glucose Sensing ◽  
Β Cell ◽  
Cell Glucose

The identification of diabetes genes mediating β-cell loss and hyperglycemia using positional cloning

2018 ◽  
Author(s):  
TT Cui ◽  
N Hallahan ◽  
W Jonas ◽  
P Gottmann ◽  
M Jähnert ◽  
...  
Keyword(s):  
Positional Cloning ◽  
Cell Loss ◽  
Β Cell

Inhibition by Phenol and Phenolic Acids of Platelet Release Reaction

1973 ◽  
Vol 30 (02) ◽  
pp. 334-338 ◽  
Author(s):  
Felisa C. Molinas
Keyword(s):  
Renal Failure ◽  
Phenolic Compounds ◽  
Phenolic Acids ◽  
Platelet Function ◽  
Deleterious Effect ◽  
Release Reaction ◽  
Contributory Factors ◽  
Adp Release ◽  
Platelet Release

SummaryIt has been postulated that the high phenol and phenolic acids plasmatic levels found in patients with chronic renal failure are contributory factors in the abnormal platelet function described in these patients. This hypothesis was corroborated by “in vitro” studies showing the deleterious effect of these compounds on certain platelet function after pre-incubation of PRP with phenol and phenolic compounds. The present studies were conducted to determine the influence of phenolic compounds on platelet release reaction. It was found that phenol inhibited from 62.5 to 100% the effect of the aggregating agents thrombin, adrenaline and ADP on platelet 5-HT-14C release. The phenolic acids p-, m-, and o-HPAA inhibited from 36.35 to 94.8% adrenaline and ADP-induced platelet 5-HT-14C release. Adrenaline-induced platelet ADP release was inhibited from 27.45 to 38.10% by the phenolic compounds. These findings confirm the hypothesis that phenolic compounds interfere with platelet function through the inhibition of the release reaction.

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