10 Questions
What is the role of TNF-a in cachexia?
Suppressing appetite
Which cells produce TNF-a?
Macrophages and some neoplastic cells
What is the effect of TNF-a on basal metabolic rate?
Increases it
What is the result of ubiquitin-proteasome degradation of skeletal muscle?
Breakdown of skeletal muscle
What is a common symptom of cancer-related cachexia?
Anorexia
What is the primary mechanism by which TNF-a contributes to weight loss in cancer-related cachexia?
Inducing anorexia through hypothalamic influences
Which of the following is a consequence of the hypermetabolic state in cancer-related cachexia?
Elevated basal metabolic rate
What is the primary function of macrophages in relation to TNF-a production?
To respond to infection by producing TNF-a
What is the result of the degradation of actin and myosin in skeletal muscle?
Muscle wasting
Which of the following is a characteristic of neoplastic cells that contributes to cancer-related cachexia?
Their ability to produce TNF-a
Study Notes
Cancer-Related Cachexia
- Cachexia is a hypermetabolic state driven by TNF-a and IL-6
- Characterized by anorexia, malaise, weight loss, and anemia
- TNF-a is produced by macrophages in response to infection and by some neoplastic cells
- TNF-a influences the hypothalamus, leading to appetite suppression
- TNF-a increases basal metabolic rate
- Ubiquitin-proteasome degradation of skeletal muscle proteins, including actin and myosin, contributes to muscle wasting in cancer-related cachexia
Cancer-Related Cachexia
- Cachexia is a hypermetabolic state driven by TNF-a and IL-6
- Characterized by anorexia, malaise, weight loss, and anemia
- TNF-a is produced by macrophages in response to infection and by some neoplastic cells
- TNF-a influences the hypothalamus, leading to appetite suppression
- TNF-a increases basal metabolic rate
- Ubiquitin-proteasome degradation of skeletal muscle proteins, including actin and myosin, contributes to muscle wasting in cancer-related cachexia
Explore the biochemistry of cancer-related cachexia, including the role of TNF-a, IL-6, and ubiquitin-proteasome degradation in skeletal muscle loss. Learn about the hypermetabolic state and its effects on the body.
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