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Related Concept Videos

Overview of Lipid Metabolism01:24

Overview of Lipid Metabolism

Lipid metabolism is a crucial process in the human body that involves the synthesis and degradation of lipids. This process is essential for energy production, cell membrane formation, and hormone production, among other functions.
Lipolysis: The Breakdown of Lipids:
Lipolysis is the process of breaking down lipids, particularly triglycerides, into glycerol and fatty acids. This process typically occurs in the adipose tissue and is triggered by various hormones, including glucagon and...
Overview of Carbohydrate Metabolism01:19

Overview of Carbohydrate Metabolism

Carbohydrate metabolism is a fundamental biochemical process that ensures a constant supply of energy to living cells. The most important carbohydrate is glucose, which can be broken down via glycolysis to enter into the Krebs cycle and eventually lead to the production of ATP through oxidative phosphorylation.
Glucose transport into cells is facilitated by a family of transport proteins called GLUT (Glucose Transporters). GLUT4 is the primary glucose transporter for insulin-stimulated glucose...
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are typically...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

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...
Metabolic States of the Body: The Postabsorptive State01:18

Metabolic States of the Body: The Postabsorptive State

The postabsorptive state usually starts about four hours after a meal and lasts until the next meal is eaten. During this time, the digestive system stops absorbing nutrients, and the body uses stored energy reserves to maintain stable blood glucose levels.
Initially, glycogen stored in the liver is broken down to release glucose into the bloodstream, while glycogen in the muscles is broken down to supply glucose for energy directly within the muscle cells. As glycogen stores diminish,...
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.

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Updated: May 9, 2026

Arteriovenous Metabolomics to Measure In Vivo Metabolite Exchange in Brown Adipose Tissue
02:55

Arteriovenous Metabolomics to Measure In Vivo Metabolite Exchange in Brown Adipose Tissue

Published on: October 6, 2023

Methylglyoxal further impairs adipose tissue metabolism after partial decrease of blood supply.

Tiago Rodrigues1, Paulo Matafome, Raquel Seiça

  • 1Laboratory of Physiology, Institute of Biomedical Imaging and Life Sciences (IBILI), Faculty of Medicine, University of Coimbra , Portugal.

Archives of Physiology and Biochemistry
|July 13, 2013
PubMed
Summary
This summary is machine-generated.

Methylglyoxal-induced glycation worsens adipose tissue dysfunction during decreased blood supply. This impairs metabolic adaptation, increasing harmful lipid levels and reducing beneficial adiponectin.

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Last Updated: May 9, 2026

Arteriovenous Metabolomics to Measure In Vivo Metabolite Exchange in Brown Adipose Tissue
02:55

Arteriovenous Metabolomics to Measure In Vivo Metabolite Exchange in Brown Adipose Tissue

Published on: October 6, 2023

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
09:41

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

Published on: March 17, 2023

Area of Science:

  • Metabolic Syndrome
  • Adipose Tissue Biology
  • Vascular Physiology

Background:

  • Methylglyoxal (MGO) causes adipose tissue lesions and vascular dysfunction.
  • Partially decreased adipose tissue irrigation is common in obesity.
  • The role of MGO in metabolic adaptation to reduced blood supply is unclear.

Purpose of the Study:

  • To investigate the impact of MGO on metabolic adaptations in partially irrigated adipose tissue.
  • To assess changes 1 and 48 hours after decreased blood supply.

Main Methods:

  • Developed a model of partially decreased adipose tissue irrigation in Wistar rats.
  • Administered methylglyoxal to rats.
  • Measured key metabolic and cellular markers at 1 and 48 hours.

Main Results:

  • Short-term (1 hour) MGO exposure increased ERK1/2 activation and degraded Ikappa-Balpha and Perilipin A.
  • Long-term (48 hours) MGO exposure led to higher fasting glucose and insulin, elevated free fatty acids and triglycerides, and reduced adiponectin.
  • These metabolic changes were linked to decreased PPARgamma levels in the affected adipose tissue.

Conclusions:

  • Glycation by methylglyoxal exacerbates metabolic dysfunction in adipose tissue experiencing reduced blood supply.
  • MGO contributes to impaired adipocyte metabolism, hindering adaptation during tissue expansion.
  • These findings highlight MGO's detrimental role in conditions like obesity with compromised tissue perfusion.