Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Outcomes of robotic lateral duodenoduodenostomy surgery for neonatal duodenal obstruction.

Surgical endoscopy·2026
Same author

ODC1-Mediated Ornithine Metabolism Exacerbates Obesity by Disrupting AMPK/ACC Pathway.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology·2026
Same author

Mitigating bioaerosol exposure risks in high-traffic clinics: Experimental and numerical optimization of air purifier interventions.

Journal of hazardous materials·2026
Same author

Global landscape of alternative polyadenylation during the growth and development of skeletal muscle in pigs.

BMC genomics·2026
Same author

Integrated analysis of transcriptome, metabolome, and lipidome revealed key genes associated with meat quality traits in pigs.

BMC genomics·2026
Same author

Differentiation of biliary atresia using a rapid point-of-care matrix metalloproteinase-7 assay: A multicenter diagnostic study.

Hepatology communications·2026

Related Experiment Video

Updated: May 30, 2026

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion
08:22

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion

Published on: March 20, 2017

Reducing plasma membrane sphingomyelin increases insulin sensitivity.

Zhiqiang Li1, Hongqi Zhang, Jing Liu

  • 1Department of Cell Biology, SUNY Downstate Medical Center, 450 Clarkson Ave. Box 5, Brooklyn, NY 11203, USA.

Molecular and Cellular Biology
|August 17, 2011
PubMed
Summary
This summary is machine-generated.

Inhibiting sphingolipid synthesis improves insulin sensitivity. Gene knockout models show reduced sphingomyelin levels enhance insulin sensitivity and protect against obesity and insulin resistance.

More Related Videos

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
08:03

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes

Published on: June 25, 2017

Related Experiment Videos

Last Updated: May 30, 2026

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion
08:22

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion

Published on: March 20, 2017

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
08:03

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes

Published on: June 25, 2017

Area of Science:

  • Biochemistry
  • Metabolic Diseases
  • Molecular Biology

Background:

  • De novo sphingolipid synthesis inhibition enhances insulin sensitivity.
  • Sphingolipids play a crucial role in metabolic regulation.
  • Understanding the precise mechanisms is vital for therapeutic development.

Purpose of the Study:

  • To investigate the role of serine palmitoyltransferase (SPT) subunit 2 (Sptlc2) and sphingomyelin synthase 2 (Sms2) in insulin sensitivity.
  • To elucidate the impact of altered sphingolipid metabolism on obesity and insulin resistance.

Main Methods:

  • Utilized heterozygous Sptlc2 gene knockout mice.
  • Utilized sphingomyelin synthase 2 (Sms2) gene knockout mice.
  • Analyzed ceramide and sphingomyelin levels in plasma membranes.
  • Assessed insulin sensitivity and response to high-fat diet.

Main Results:

  • Heterozygous Sptlc2 deficiency decreased ceramide and sphingomyelin levels, increasing insulin sensitivity.
  • Sms2 deficiency decreased sphingomyelin levels, increasing insulin sensitivity.
  • Both Sptlc2 heterozygous and Sms2 deficient mice showed protection against high-fat diet-induced obesity and insulin resistance.

Conclusions:

  • Reduced sphingomyelin levels in plasma membranes improve tissue and whole-body insulin sensitivity.
  • Targeting Sptlc2 or Sms2 offers a potential therapeutic strategy for metabolic disorders.
  • Sphingolipid metabolism is a key regulator of insulin sensitivity and energy balance.