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Related Concept Videos

Amino Acid Biosynthetic Pathways01:29

Amino Acid Biosynthetic Pathways

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Amino acid biosynthesis is essential for cell growth, protein synthesis, and metabolic regulation. Cells generate essential and non-essential amino acids from metabolic intermediates to sustain vital biological functions. These intermediates originate from key metabolic pathways: glycolysis, the tricarboxylic acid (TCA) cycle, and the pentose phosphate pathway. Important precursors include α-ketoglutarate, pyruvate, oxaloacetate, phosphoenolpyruvate, and erythrose-4-phosphate, which...
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Carboxylic Acids to Primary Alcohols: Hydride Reduction01:17

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Carboxylic acids, upon reaction with strong reducing agents such as lithium aluminum hydride followed by hydrolysis, undergo reduction to form primary alcohols.
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Acid Halides to Alcohols: LiAlH4 Reduction01:19

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Acid halides are reduced to alcohols in the presence of a strong reducing agent like lithium aluminum hydride.
The mechanism proceeds in three steps. First, the nucleophilic hydride ion attacks the carbonyl carbon of the acid halide to form a tetrahedral intermediate. Next, the carbonyl group is re-formed, and the halide ion departs as a leaving group, generating an aldehyde. A second nucleophilic attack by the hydride yields an alkoxide ion, which, upon protonation, gives a primary alcohol as...
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Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Induced-fit Model01:13

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Most chemical reactions in cells require enzymes—biological catalysts that speed up the reaction without being consumed or permanently changed. They reduce the activation energy needed to convert the reactants into products. Enzymes are proteins, that usually work by binding to a substrate—a reactant molecule that they act upon.
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C4 Pathway and CAM01:27

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Most plants use the C3 pathway for carbon fixation. However, some plants, such as sugar cane, corn, and cacti that grow in hot conditions, use alternative pathways to fix carbon and conserve energy loss due to photorespiration. Photorespiration is the process that occurs when the oxygen concentration is high. Under such conditions, the rubisco enzyme in the Calvin cycle binds O2 instead of CO2, which halts photosynthesis and consumes energy.
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Related Experiment Video

Updated: Jan 29, 2026

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
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Ellagic Acid Alleviates Abnormal Fat Reduction by Activating the RXRβ-PPARγ Pathways in a CT26 Tumour-Induced

Woo Yong Park1,2, Beomsu Kim3, Gahee Song1,2

  • 1Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.

Journal of Cachexia, Sarcopenia and Muscle
|January 28, 2026
PubMed
Summary
This summary is machine-generated.

Ellagic acid (EA) effectively combats cancer cachexia by preventing fat loss and improving body composition. This natural compound activates the RXRβ-PPARγ pathway, offering a potential therapeutic strategy for cachexia-related symptoms.

Keywords:
PPARγRXRβabnormal fat reductioncancer cachexiaellagic acid

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Cancer cachexia is a severe metabolic syndrome characterized by significant weight loss, impacting patient survival.
  • Current pharmacological interventions for cancer cachexia are limited, particularly for mitigating abnormal fat reduction.

Purpose of the Study:

  • To investigate the potential of ellagic acid (EA) in preventing and treating cancer-induced fat loss.
  • To elucidate the molecular mechanisms underlying EA's effects on adipogenesis and cachexia.

Main Methods:

  • In vitro studies using 3T3-L1 adipocytes exposed to cancer cell conditioned medium to simulate cachexia.
  • In vivo studies utilizing a CT26 colon cancer-induced cachexia mouse model treated with varying doses of EA.
  • Analysis of lipid accumulation, adipogenesis markers (PPARγ, RXRβ, C/EBPα, SREBP1), and molecular mechanisms including gene silencing and docking.

Main Results:

  • EA treatment restored lipid accumulation in vitro and upregulated PPARγ and RXRβ expression, an effect dependent on RXRβ.
  • In vivo, EA administration significantly improved physical performance, increased inguinal white adipose tissue (iWAT) mass, and enhanced tumor-free body weight.
  • EA treatment increased adipogenesis-related protein expression in iWAT and promoted RXRβ nuclear localization without affecting tumor growth.

Conclusions:

  • Ellagic acid mitigates cancer cachexia-induced fat loss by activating the RXRβ-PPARγ pathway.
  • EA demonstrates potential as a pharmacological agent to address abnormal fat reduction and associated muscle dysfunction in cachexia.
  • These findings highlight EA as a promising therapeutic candidate for managing cancer cachexia.