The major factors controlling gut function are autonomic reflexes, the enteric nervous system, and the hormones gastrin, secretin, and cholecystokinin. Insulin is the major hormonal controller of fuel metabolism through its effects on liver, muscle, and adipose tissues. The hypothalamus controls food intake by generating sensations of hunger and satiety influenced by feedback from blood glucose and hormones, including insulin, leptin, and ghrelin.
learning outcomes
You should be able to:
Explain how hormones control the rate of delivery of substrate to the small intestine and the appropriate secretions of digestive juices.
Describe metabolic interconversions that take place in liver and muscle to meet the body’s demands for glucose.
Differentiate between the classes of lipoproteins.
Compare the effects of insulin on activities in skeletal muscle cells, adipose cells, and liver cells.
Cite evidence that supports the role of leptin as a satiety signal and ghrelin as a hunger signal.
Interpret results from experiments designed to elucidate the mechanisms underlying regulation of body mass and food intake behaviors.
For various reasons patients may be fed through a tube going into their stomachs or tubes going all the way to their jejunum, the middle region of their small intestines. How would the feeding formulas used in the jejunal tube have to differ from the one applied through the gastric tube?
Introducing nutrient solutions into the jejunum would not stimulate release of secretin or CCK, therefore there would not be bile secretion to emulsify large complex lipids and there would not be pancreatic enzymes to digest complex carbohydrates and proteins. Thus, the jejunal formula would have to consist of medium to short chain fatty acids and partially hydrolyzed carbohydrates and proteins.
How do the three classes of lipoproteins differ in structure and function?
The three classes of lipoproteins differ in their relative compositions of protein, triglycerides, and cholesterol. The high-
How are the effects of high and low insulin levels the same and different in liver and muscle?
In both muscle and liver, insulin promotes the uptake of glucose and its incorporation into glycogen. When insulin levels fall, the effects are different in liver and muscle, in that in liver the reduced levels activate glucose phosphatase. This makes it possible for the glucose produced by the breakdown of glycogen to be released into the interstitial fluid. This process does not occur in muscle, so the glucose is trapped in the muscle.
In the experiments in which the lateral or the ventromedial hypothalamus was lesioned, what result enabled the conclusion that the regulation of body mass was altered rather than just the ability to produce satiety or hunger by the nutritional state of the body?
In the experiments in which the lateral hypothalamus or the ventromedial hypothalamus was lesioned and subsequent changes in body mass measured, the animals either gained or lost a large amount of mass, but they eventually plateaued at a new level, indicating the continued ability to regulate, but at a different level.
When exercising muscles do not have an adequate supply of oxygen, they continue to produce small amounts of ATP through glycolysis, but they also produce pyruvate and lactate. Explain how this pyruvate and lactate can help support continuing glycolysis.
Pyruvate and lactate produced by muscles working anaerobically enter the circulation and are taken up by the liver, where they are converted to glucose by processes of gluconeogenesis. This glucose can then return to the blood and support further glycolysis by the muscles.
What evidence supports the hypothesis that leptin influences satiety?
Rats that have a mutation that eliminates their production of leptin eat more and become obese. If these rats are joined parabiotically with normal rats that produce leptin, the obese rats eat less and lose mass.