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Related Concept Videos

Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
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 I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: Dosing Regimen and Adverse Effects

Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
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: Management and Pharmacotherapy01:15

Diabetes: Management and Pharmacotherapy

The therapy for diabetes aims to alleviate hyperglycemia-related symptoms, prevent acute metabolic decompensation, and reduce chronic end-organ complications. Glycemic control is evaluated through short-term (self-monitoring, continuous glucose monitoring) and long-term (A1c, fructosamine) metrics, enabling near real-time tracking of blood glucose levels and reflecting glycemic control over specific time frames.
Insulin remains the cornerstone of treatment for most patients with type 1 and many...

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A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
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Beta cell function during rapamycin monotherapy in long-term type 1 diabetes.

L Piemonti1, P Maffi, L Monti

  • 1Diabetes Research Institute (HSR-DRI), San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy. piemonti.lorenzo@hsr.it

Diabetologia
|November 4, 2010
PubMed
Summary
This summary is machine-generated.

Rapamycin monotherapy may reinstate beta cell function in long-term type 1 diabetes patients. This immunosuppression therapy increased C-peptide levels and decreased insulin antibody titres, suggesting potential for beta cell recovery.

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Area of Science:

  • Endocrinology
  • Immunology
  • Metabolic Diseases

Background:

  • Type 1 diabetes is typically considered irreversible at end-stage disease.
  • Residual beta cell function may exist if autoimmunity is controlled.
  • Investigating therapies to restore beta cell function is crucial.

Purpose of the Study:

  • To determine if immunosuppression therapy can reinstate beta cell function in patients with long-term type 1 diabetes.
  • To assess the effect of rapamycin monotherapy on beta cell function and autoimmunity markers.

Main Methods:

  • Examined pancreatic beta cell function in 22 patients with long-term type 1 diabetes receiving rapamycin monotherapy.
  • Measured fasting C-peptide, insulin antibody titre, and serum proinsulin levels.
  • Compared outcomes with 14 control patients awaiting islet transplantation without rapamycin.

Main Results:

  • Fasting C-peptide increased significantly in patients on rapamycin (p < 0.005).
  • 12 patients showed increased C-peptide levels, indicating response.
  • Rapamycin reduced insulin antibody titres (p < 0.001) and serum proinsulin (p = 0.001).

Conclusions:

  • Immunosuppression therapy, specifically rapamycin, may restore beta cell function in long-term type 1 diabetes.
  • These findings suggest potential therapeutic strategies for C-peptide-negative type 1 diabetes patients.
  • Further research into reinstating beta cell function is warranted.