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

Regulation of Food Intake01:30

Regulation of Food Intake

2.8K
Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
2.8K
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

8
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.
8
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

1.3K
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...
1.3K
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

10
Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH...
10
Hyperosmolar Hyperglycemic State01:21

Hyperosmolar Hyperglycemic State

11
Hyperosmolar Hyperglycemic State, or HHS, is a serious and life-threatening complication of type 2 diabetes mellitus. It is characterized by three main features: severe hyperglycemia, profound dehydration, and elevated serum osmolality, all occurring without significant ketoacidosis.HHS typically develops in older adults or individuals with limited access to fluids. This may result from illness, cognitive impairment, or medications such as diuretics or corticosteroids. These factors reduce...
11
Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

9
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...
9

You might also read

Related Articles

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

Sort by
Same author

Tumor treating fields combined with concurrent chemoradiotherapy for glioblastoma: A multi-institutional analysis.

iScience·2026
Same author

Neoadjuvant retlirafusp alfa (anti-PD-L1/TGF-β bifunctional fusion protein) with or without chemotherapy in unresectable stage III non-small cell lung cancer: updated results from the phase 2 TRAILBLAZER trial.

Signal transduction and targeted therapy·2026
Same author

Flotation Separation of Spodumene from Feldspar with Combined Collectors: Experimental and Molecular Dynamics Simulation Studies.

Langmuir : the ACS journal of surfaces and colloids·2026
Same author

Van der Waals strain hardening and large uniform tensile elongation in GaSe.

Nature materials·2026
Same author

In a Rodent Model, Low-Dose Maternal Magnesium Sulfate Achieves Comparable Neuroinflammatory Attenuation to Higher Dose.

American journal of obstetrics and gynecology·2026
Same author

Plastic-Deformation-Free Fabrication of Freestanding Metal Chalcogenide Ribbons for High-Performance Flexible Thermoelectric Generators.

Advanced materials (Deerfield Beach, Fla.)·2026

Related Experiment Video

Updated: Apr 23, 2026

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
11:36

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood

Published on: April 28, 2016

9.3K

Programmed hyperphagia secondary to increased hypothalamic SIRT1.

Mina Desai1, Tie Li1, Guang Han1

  • 1Perinatal Research Laboratories, Department of Obstetrics and Gynecology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California 90502.

Brain Research
|September 24, 2014
PubMed
Summary
This summary is machine-generated.

Small for gestational age (SGA) offspring develop obesity due to impaired hypothalamic satiety pathways. Elevated SIRT1 in SGA newborns causes premature neuroprogenitor cell differentiation, reducing the neural pool and promoting hyperphagia.

Keywords:
Appetite and satiety neuropeptidesHypothalamic neuroprogenitor cellsProliferation and differentiationSirtinol and resveratrolbHLH genes

More Related Videos

Control of Eating Behavior Using a Novel Feedback System
04:48

Control of Eating Behavior Using a Novel Feedback System

Published on: May 8, 2018

11.9K
Fat Preference: A Novel Model of Eating Behavior in Rats
05:57

Fat Preference: A Novel Model of Eating Behavior in Rats

Published on: June 27, 2014

13.0K

Related Experiment Videos

Last Updated: Apr 23, 2026

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
11:36

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood

Published on: April 28, 2016

9.3K
Control of Eating Behavior Using a Novel Feedback System
04:48

Control of Eating Behavior Using a Novel Feedback System

Published on: May 8, 2018

11.9K
Fat Preference: A Novel Model of Eating Behavior in Rats
05:57

Fat Preference: A Novel Model of Eating Behavior in Rats

Published on: June 27, 2014

13.0K

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Endocrinology

Background:

  • Small for gestational age (SGA) offspring are predisposed to hyperphagia and adult obesity.
  • This is linked to reduced hypothalamic neural satiety pathways, specifically within the arcuate nucleus (ARC).
  • Neuroprogenitor cell (NPC) proliferation and differentiation are critical for ARC development.

Purpose of the Study:

  • To investigate the role of SIRT1 in the altered hypothalamic development of SGA offspring.
  • To determine the impact of SIRT1 on NPC proliferation and differentiation in the context of SGA.
  • To elucidate the molecular mechanisms linking SGA, SIRT1, and hypothalamic neuronal development.

Main Methods:

  • In vivo studies of SGA and control offspring.
  • In vitro culture of hypothalamic neuroprogenitor cells (NPCs).
  • Analysis of protein and gene expression (SIRT1, AgRP, POMC, Hes1, Mash1, neurogenin3, Tuj1).
  • SIRT1 manipulation using siRNA and pharmacological agents.

Main Results:

  • SGA offspring exhibited increased hypothalamic/ARC SIRT1 and AgRP, with decreased POMC.
  • SGA newborns showed reduced hypothalamic neurogenic factors and in vivo NPC proliferation.
  • In vitro, elevated SIRT1 in SGA NPCs correlated with reduced proliferation and premature differentiation; SIRT1 inhibition rescued these deficits.
  • SIRT1 directly impacts NPC proliferation and differentiation, with elevated levels in SGA inducing premature differentiation.

Conclusions:

  • Elevated SIRT1 in SGA newborns contributes to reduced NPC proliferation and premature differentiation.
  • This process diminishes the neuroprogenitor cell pool, potentially programming hyperphagia and adult obesity.
  • SIRT1 is a key mediator linking nutritional status during gestation to long-term hypothalamic development and metabolic programming.