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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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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...
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GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Related Experiment Video

Updated: Jul 19, 2025

Body Composition and Metabolic Caging Analysis in High Fat Fed Mice
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GIRK2 potassium channels expressed by the AgRP neurons decrease adiposity and body weight in mice.

Youjin Oh1, Eun-Seon Yoo1, Sang Hyeon Ju2

  • 1Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.

Plos Biology
|August 18, 2023
PubMed
Summary
This summary is machine-generated.

G protein-gated inwardly rectifying K+ (GIRK) channels stabilize appetite-regulating neurons. Deleting GIRK2 in these neurons increases excitability, leading to higher body weight and reduced energy expenditure, not altered food intake.

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Area of Science:

  • Neuroscience
  • Metabolism
  • Endocrinology

Background:

  • Neuropeptide Y (NPY)/agouti-related peptide (AgRP) neurons regulate appetite and energy expenditure (EE).
  • Intrinsic molecular regulators of NPY/AgRP neuronal excitability and their impact on long-term metabolic function are not fully understood.

Purpose of the Study:

  • To investigate the role of G protein-gated inwardly rectifying K+ (GIRK) channels in regulating NPY/AgRP neuronal excitability.
  • To determine the impact of GIRK2 subunit deletion in NPY/AgRP neurons on metabolic function and adaptation to environmental stress.

Main Methods:

  • Generation of NPY/AgRP neuron-selective GIRK2 knockout mice.
  • Assessment of neuronal excitability, food intake, body weight, adiposity, and sympathetic activity.
  • Evaluation of cold stress adaptation.

Main Results:

  • NPY/AgRP neuron-selective deletion of GIRK2 led to persistently increased neuronal excitability.
  • GIRK2 knockout mice exhibited increased body weight and adiposity due to decreased sympathetic activity and EE, with unchanged food intake.
  • Conditional knockout mice showed impaired adaptation to cold conditions.

Conclusions:

  • GIRK2 is a critical determinant of NPY/AgRP neuronal excitability.
  • GIRK2 plays a key role in regulating energy expenditure under physiological and stress conditions.