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Related Concept Videos

Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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Diabetes: Symptoms, Diagnosis, and Complications01:15

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For most patients, experiencing several weeks of polyuria, polydipsia, fatigue, and significant weight loss may indicate the presence of diabetes. Furthermore, adults displaying the phenotypic appearance of type 2 diabetes (particularly those who are obese and not initially insulin-requiring), may have islet cell autoantibodies, suggesting autoimmune-mediated β cell destruction and a diagnosis of latent autoimmune diabetes of adults (LADA). The categorization of glucose homeostasis is...
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Diabetes Mellitus: Type 2 and Gestational01:22

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Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
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Diabetes Mellitus: Overview and Type I Subtype01:22

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Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
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Hypoglycemia and Glucagon01:15

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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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Carbohydrate Metabolism01:36

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Carbohydrates are polymers composed of molecules containing atoms of carbon, hydrogen and oxygen. One gram of carbohydrate can provide four kilo-calories of energy, which makes it the most efficient instant energy source.
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Updated: Aug 27, 2025

Isolation of Human Islets from Partially Pancreatectomized Patients
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Hepatogenous diabetes: Knowledge, evidence, and skepticism.

Ramesh Kumar1, Diego García-Compeán2, Tanmoy Maji3

  • 1Department of Gastroenterology, All India Institute of Medical Sciences, Patna 801507, Bihar, India. docrameshkr@gmail.com.

World Journal of Hepatology
|September 26, 2022
PubMed
Summary

Hepatogenous diabetes (HD), a form of diabetes mellitus resulting from liver cirrhosis, affects 21-57% of patients. Its distinct pathophysiology, involving insulin resistance and beta-cell dysfunction, warrants recognition as a separate entity.

Keywords:
CirrhosisDiabetesGlucose intoleranceHepatogenous diabetesInsulin resistanceMetabolism

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Area of Science:

  • Endocrinology
  • Hepatology
  • Metabolic Disorders

Background:

  • Liver cirrhosis (LC) is linked to diabetes mellitus (DM), termed hepatogenous diabetes (HD).
  • HD prevalence in LC patients ranges from 21% to 57%.
  • Existing research often fails to distinguish HD from type 2 diabetes mellitus (T2DM) in LC patients.

Purpose of the Study:

  • To review the distinct pathophysiological basis of HD.
  • To discuss the clinical and therapeutic implications of HD.
  • To address skepticism regarding HD as a separate disease entity.

Main Methods:

  • Literature review of studies on liver cirrhosis and diabetes.
  • Analysis of pathophysiological mechanisms linking LC to glucose metabolism dysfunction.
  • Examination of clinical outcomes and treatment approaches for HD.

Main Results:

  • HD pathophysiology involves insulin resistance and pancreatic beta-cell dysfunction, exacerbated by LC-related factors like inflammation and endotoxemia.
  • Factors such as sarcopenia, gut dysbiosis, and hyperammonemia contribute to impaired glucose metabolism in LC.
  • Current treatment for HD often mirrors T2DM management, despite potential differences in pathophysiology.

Conclusions:

  • HD is a distinct diabetes entity with significant prevalence and a unique pathophysiological basis.
  • Further research is needed to clarify the individual impact of HD versus T2DM on LC outcomes.
  • Standardized diagnostic criteria and tailored therapeutic guidelines for HD are necessary.