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Chapter 22: Q15CP (page 790)

How does thermogenesis help prevent obesity?

Short Answer

Expert verified

Obesity is prevented by thermogenesis as it burns the fat molecule and converts it into heat energy.

Step by step solution

01

Obesity

Obesity is the excess body fat associated with a significant increase in mortality and reduced life expectancy by up to ten years. It is measured by body mass index (BMI).

02

Preventing obesity

The body prevents obesity by thermogenesis, i.e., production of heat which is increased by a high energy intake.

The beige fat cells play a role in preventing obesity, and exercising muscle promotes the development of beige adipocytes by releasing an irisin (112-residue peptide hormone).

Exercise helps to reduce weight gain by using two methods:

  • Using food calories to power muscle contraction.
  • Promoting the conversion of excess calories to heat rather than fat.

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Most popular questions from this chapter

The passive glucose transporter named GLUT1 (Fig. 10-13) is present in the membranes of many cells, but not in the liver. Instead, liver cells express the GLUT2 transporter, which exhibits different transport kinetics. Given what you know about the role of the liver in buffering blood glucose, compare the KMvalues of GLUT1 and GLUT2.

High concentrations of free fatty acids in the blood are known to cause insulin resistance in muscle, but only after 5 hours. This suggests that a metabolite of the fatty acids may be responsible for this phenomenon. It is also known that an isoform of protein kinase C is activated during the process and that high concentrations of free fatty acids result in intramuscular accumulation of triacylglycerols. With this information, review the mechanism of activation of PKC and the pathway of triacylglycerol biosynthesis and suggest a metabolite that may be responsible for PKC activation.

Summarize the role of insulin in regulating fuel metabolism in the liver, muscle, and adipose tissue.

Pancreatic βcells express a receptor for fatty acids. Fatty acid binding to the protein appears to stimulate insulin secretion. Does this phenomenon make metabolic sense?

When administered intravenously, the peptide hormonePYY3-36 sometimes triggers nausea in humans. Is this consistent with its biological function?
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