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Related Concept Videos

Cushing Syndrome I: Introduction01:26

Cushing Syndrome I: Introduction

Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...
Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Type I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
Diabetes Mellitus: Introduction01:26

Diabetes Mellitus: Introduction

Diabetes mellitus consists of chronic metabolic disorders characterized by persistent hyperglycemia. This elevated blood glucose results from defects in insulin secretion, impaired insulin action, or both. Insulin, produced by pancreatic β-cells, is essential for maintaining glucose homeostasis by facilitating cellular glucose uptake for energy or storage. Disruptions in insulin production or function lead to glucose accumulation in the bloodstream, causing the clinical features and long-term...
Pathophysiology of Diabetes01:20

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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.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...

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Related Experiment Video

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Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
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Diabetes in Cushing syndrome: basic and clinical aspects.

Gherardo Mazziotti1, Carmine Gazzaruso, Andrea Giustina

  • 1Department of Medical and Surgical Sciences University of Brescia, Endocrine Service, Montichiari Hospital, 25018, Brescia, Italy.

Trends in Endocrinology and Metabolism: TEM
|October 14, 2011
PubMed
Summary

Cushing syndrome (CS) frequently causes diabetes due to excess glucocorticoids, leading to insulin resistance. Managing CS and diabetes involves controlling hyperglycemia and correcting the underlying glucocorticoid excess.

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Area of Science:

  • Endocrinology
  • Metabolic Disorders

Background:

  • Cushing syndrome (CS) results from chronic glucocorticoid excess.
  • CS presents with symptoms like central obesity, purple striae, and muscle weakness.
  • Diabetes mellitus is a common complication of CS.

Purpose of the Study:

  • To review glucose metabolism disorders in patients with glucocorticoid excess.
  • To explore the pathophysiological mechanisms linking glucocorticoids and diabetes.
  • To discuss clinical and therapeutic implications for managing CS and diabetes.

Main Methods:

  • Literature review of studies on Cushing syndrome and diabetes mellitus.
  • Analysis of pathophysiological mechanisms of glucocorticoid-induced insulin resistance and impaired insulin secretion.
  • Synthesis of clinical and therapeutic strategies for hyperglycemia management in CS patients.

Main Results:

  • Glucocorticoid excess induces insulin resistance and impairs insulin secretion, leading to diabetes mellitus.
  • Hyperglycemia is a hallmark of CS-associated diabetes.
  • Correction of glucocorticoid excess is a key therapeutic goal.

Conclusions:

  • Diabetes mellitus is a frequent and significant complication of Cushing syndrome.
  • Understanding the pathophysiology is crucial for effective management.
  • Integrated treatment strategies addressing hyperglycemia and glucocorticoid excess are essential.