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Chapter 16
acid concentrations increase in the blood after ingestion of a
protein-containing meal, and the increased plasma insulin stim-
ulates the uptake of these amino acids by muscle and other cells,
thereby lowering their concentrations.
There are also important hormonal controls over insulin
secretion. For example, a hormone—glucose-dependent insu-
linotropic peptide (GIP)—secreted by endocrine cells in the
gastrointestinal tract in response to eating stimulates the release
of insulin. This response provides a feedforward component to
glucose regulation during the ingestion of a meal. Thus, insulin
secretion rises earlier than it would have if plasma glucose were
the only controller, thereby minimizing the peak in plasma glu-
cose concentration. This mechanism minimizes the likelihood
of large increases in plasma glucose after a meal.
Finally, the autonomic neurons to the islets of Langerhans
also infl uence insulin secretion. Activation of the parasympa-
thetic neurons, which occurs during the ingestion of a meal,
stimulates the secretion of insulin and constitutes a second
type of feedforward regulation. In contrast, activation of the
sympathetic neurons to the islets or an increase in the plasma
concentration of epinephrine (the hormone secreted by the
adrenal medulla) inhibits insulin secretion. The signifi cance of
this relationship for the body’s response to low plasma glucose
(
hypoglycemia
), stress, and exercise—all situations in which
sympathetic activity is increased—will be described later in
this chapter.
In summary, insulin plays the primary role in control-
ling the metabolic adjustments required for feasting or fasting.
Other hormonal and neural factors, however, also play signifi -
cant roles. They all oppose the action of insulin in one way or
another and are known as
glucose-counterregulatory con-
trols.
As described next, the most important of these are glu-
cagon, epinephrine, sympathetic nerves, cortisol, and growth
hormone.
Glycogen
Glucose
Glucose
utilization
Amino
acids
Proteins
Muscle
Adipocytes
Glycogen
Glucose-6-phosphate
Pyruvate
Amino
acids
Acetyl CoA
Glucose
Ketones
Fatty
acids
Glucose
Amino
acids
Glucose
Glucose
Glucose
Fatty acids
α
-glycerol-
phosphate
Triglycerides
Glycerol
Fatty acids
and
monoglycerides
Triglycerides
Lipoprotein
lipase
Blood
Liver
Figure 16–6
Illustration of the key biochemical events that underlie the responses
of target cells to insulin as summarized in Figure 16–4. Each green
arrow denotes a process stimulated by insulin, whereas a dashed red
arrow denotes inhibition by insulin. Except for the effects on the
transport proteins for glucose and amino acids, all other effects are
exerted on insulin-sensitive enzymes. The bowed arrows denote
pathways whose reversibility is mediated by different enzymes
(Chapter 3); such enzymes are commonly the ones infl uenced by
insulin and other hormones. The black arrows are processes that are
not
directly
affected by insulin, but are enhanced in the presence of
increased insulin as the result of mass action.
Begin
Restoration of plasma
glucose to normal
Plasma insulin
Adipocytes and Muscle
Glucose uptake
Pancreatic islet beta cells
Insulin secretion
Plasma glucose
Liver
Cessation of glucose output;
net glucose uptake
Figure 16–7
Nature of plasma glucose control over insulin secretion. As glucose
levels increase in plasma (e.g., after a meal containing carbohydrate),
insulin secretion is rapidly stimulated. The increase in insulin
stimulates glucose transport from extracellular fl
uid into cells, thus
decreasing plasma glucose concentrations. Insulin also acts to inhibit
hepatic glucose output.
Figure 16–7
physiological
inquiry
Notice that the brain is not listed as being insulin-sensitive. Why
is that advantageous?
Answer can be found at end of chapter.
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