Related Experiment Video
Updated: Jun 6, 2026
08:32
Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
Published on: January 4, 2018
Brainstem Hap1-Ahi1 is involved in insulin-mediated feeding control
Shao-Na Niu1, Zhen-Bo Huang, Hao Wang
1CAS Key Laboratory of Regenerative Biology, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, People's Republic of China.
FEBS Letters
|December 15, 2010
Summary
The brainstem Hap1-Ahi1 complex senses insulin signals to control feeding behavior. Its expression increases with fasting or low insulin, and decreasing it reduces food intake.
Area of Science:
- Neuroscience
- Endocrinology
- Metabolism
Background:
- The brainstem plays a crucial role in regulating feeding behavior.
- Insulin signaling is vital for metabolic control, but its brainstem mechanisms are not fully understood.
Purpose of the Study:
- To investigate the function of the Hap1-Ahi1 complex in the brainstem for feeding behavior regulation.
- To determine the role of Hap1-Ahi1 in response to metabolic cues like insulin levels.
Main Methods:
- Upregulation of Hap1-Ahi1 in mice under fasting or 2-deoxy-D-glucose (2-DG) conditions.
- Assessment of Hap1-Ahi1 expression changes following streptozotocin (STZ)-induced insulin reduction.
- Evaluation of Hap1-Ahi1 expression after intra-brain insulin injection.
- Analysis of feeding behavior and body weight changes after RNAi-mediated knockdown of brainstem Hap1.
Main Results:
- Hap1-Ahi1 expression was significantly upregulated in the brainstem during fasting or 2-DG treatment.
- Streptozotocin (STZ) administration led to a significant increase in Hap1-Ahi1.
- Intra-brain insulin injection decreased Hap1-Ahi1 expression in the brainstem.
- Knockdown of brainstem Hap1 resulted in decreased food intake and body weight.
Conclusions:
- The Hap1-Ahi1 complex in the brainstem acts as a sensor for insulin signals.
- This complex is integral to the neural regulation of feeding behavior and energy balance.
Related Concept Videos
01:30Regulation of Food Intake
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...
01:27Glucose 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...
Insulin and C-peptide are co-secreted in...
01:28Insulin: 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...
01:16Hormones 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...
In addition to accelerating glucose uptake and utilization, insulin has...
01:01Feedback Loops
In most cases, excessive hormone production is prevented by negative feedback—a loop that starts with a stimulus inducing the release of a particular substance, like a hormone, to maintain a certain level before triggering a signal that results in a decrease in further release of the hormone.
01:15Hypoglycemia 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...