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Related Concept Videos

Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
Obesity01:24

Obesity

The Body Mass Index (BMI) is a numerical value derived from a person's weight and height, used to categorize individuals into weight ranges. It is calculated using the formula: weight in kilograms divided by height in meters squared. Obesity is a health condition characterized by excessive accumulation of adipose tissue that poses health risks, often diagnosed with a BMI ≥ 30. This excess fat storage occurs when surplus dietary calories are converted into triglycerides and stored in adipocytes...

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Related Experiment Video

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White and Brown Adipose Grafts: An Approach to Correct Reproductive, Metabolic, and Renal Deficits in Black and Tan Brachyury (BTBR) Obese Mice
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Obesity development in caspase-1-deficient mice.

H Wang1, W Capell1, J H Yoon1

  • 1Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

International Journal of Obesity (2005)
|May 22, 2013
PubMed
Summary
This summary is machine-generated.

Mice lacking caspase-1 (an enzyme involved in inflammation) developed obesity, particularly males on a low-fat diet. This suggests lower interleukin-18 levels contribute to obesity development.

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Area of Science:

  • Immunology
  • Metabolism
  • Obesity Research

Background:

  • Caspase-1 is an intracellular cysteine protease crucial for inflammation by activating IL-1β and IL-18.
  • Interleukin-18 (IL-18) and IL-1β play roles in energy balance, with IL-18 deficiency linked to obesity and insulin resistance.

Purpose of the Study:

  • To investigate whether caspase-1 deficiency leads to obesity.
  • To explore the potential role of reduced IL-18 levels in caspase-1 knockout mice regarding obesity.

Main Methods:

  • Comparison of caspase-1-deficient (caspase-1-/-) and wild-type (WT) mice of both sexes.
  • Feeding mice either a high-fat (HF) or low-fat (LF) diet from 6 weeks of age.
  • Monitoring body composition and measuring plasma cytokine levels (IL-18, IL-1β).

Main Results:

  • Caspase-1-/- mice exhibited lower but detectable IL-18 levels; IL-1β was below detection limits in all groups.
  • Male caspase-1-/- mice showed increased fat mass on HF diets by 16 weeks and on LF diets by 40 weeks.
  • Female caspase-1-/- mice gained more fat on HF diets by 28 weeks, but not on LF diets.

Conclusions:

  • Caspase-1 deficiency results in obesity with age- and sex-dependent variations.
  • Male mice lacking caspase-1 develop obesity on both HF and LF diets, while females do so only on HF diets.
  • Reduced IL-18 levels in caspase-1-/- mice may contribute to obesity development, mirroring findings in IL-18-deficient mice.