Severe Hyperglycemia
Severe Hyperglycemia - Related Videos
13:35
Acute and Chronic Models of Hyperglycemia in Zebrafish: A Method to Assess the Impact of Hyperglycemia on Neurogenesis and the Biodistribution of Radiolabeled Molecules
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Cited by 25 •
2017
This work describes methods to establish acute and chronic hyperglycemia models in zebrafish. The aim is to investigate the impact of hyperglycemia on physiological processes, such as constitutive and injury-induced neurogenesis. The work also highlights the use of zebrafish to follow radiolabeled molecules (here, [18F]-FDG) using PET/CT.
01:29
Hyperglycemia
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2026
Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...
14:39
Bronchial Thermoplasty: A Novel Therapeutic Approach to Severe Asthma
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Cited by 4 •
2010
Bronchial thermoplasty is a non-drug procedure for severe persistent asthma that delivers thermal energy to the airway wall in a precisely controlled manner to reduce excessive airway smooth muscle. Reducing airway smooth muscle decreases the ability of the airways to constrict, thereby reducing the frequency of asthma attacks.
11:39
The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
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Cited by 26 •
2013
Psoriasis is a chronic, immune-mediated inflammatory skin disease. The Goeckerman regimen, formulated for the treatment of psoriasis, consists of exposure to ultraviolet B (UVB) light and application of crude coal tar (CCT). The following protocol is for the administration of Goeckerman therapy for the treatment of moderate-to-severe psoriasis.
02:28
Measuring Psoriasis Severity at Home
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2024
This paper details the creation of a Psoriasis Thickness Reference Card, enabling psoriasis patients to self-assess their psoriasis plaque thickness without the need for physician assistance. Additionally, the precision of self-assessment for psoriasis redness and scaliness by employing reference images depicting various skin tones is assessed.
FAQs
The central defect is reduced cellular glucose uptake combined with continued glucose release from the liver. When insulin is absent or ineffective, these processes work in the same direction, leaving more glucose in the bloodstream rather than directing it into cells. This relationship makes severe hyperglycemia useful for examining insulin signaling and the regulation of glucose homeostasis.
Excess blood glucose promotes osmotic diuresis, meaning glucose-related osmotic effects increase water loss. The resulting dehydration further stresses cellular and metabolic function, contributing to the potentially life-threatening nature of the disturbance. This mechanism is important when interpreting why elevated glucose is not only a concentration abnormality but also a driver of systemic fluid imbalance.
Fat breakdown becomes important when limited insulin action shifts metabolism away from normal glucose use. In some cases, this process produces ketones, creating a metabolic pattern associated with diabetic ketoacidosis. Tracking this shift helps connect impaired insulin action with downstream metabolic stress and explains why severe hyperglycemia can progress beyond excess circulating glucose alone.
In biology, severe hyperglycemia provides a model in which disrupted insulin action can be examined alongside impaired glucose uptake and continued hepatic glucose release. Researchers can use this context to relate signaling defects to changes in glucose homeostasis and cellular function. The model therefore links molecular regulation with whole-system metabolic consequences.
Pancreatic beta-cell function is relevant because these cells are connected to insulin availability, one of the central variables governing blood glucose regulation. Studying severe hyperglycemia alongside beta-cell function can help investigators examine how altered insulin production or action affects metabolic balance. This perspective supports interpretation of glucose-related disease mechanisms rather than focusing on glucose concentration alone.
Diabetic ketoacidosis and hyperosmolar states represent clinically important contexts in which the mechanisms of severe hyperglycemia become especially consequential. Understanding glucose accumulation, dehydration, and possible ketone production helps organize recognition of these states. In research and biology education, they also illustrate how a disruption in homeostasis can produce broader metabolic stress and life-threatening outcomes.