Page 297 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

!
and glycogenesis and suppresses those involved poglycemia (e.g., due to fasting, prolonged
in gluconeogenesis. Insulin also increases the physical exercise; ! B) and sympathetic im-
number of GLUT-4 uniporters in skeletal myo- pulses (via ! 2 adrenoceptors; ! A). Glucagon
cytes. All these actions serve to lower the secretion is inhibited by glucose and SIH
plasma glucose concentration (which in- (! p. 273, B) as well as by high plasma concen-
creases after food ingestion). About two-thirds trations of free fatty acids.
of the glucose absorbed by the intestines after The actions of glucagon (! A, B, C) (via
a meal (postprandial) is temporarily stored cAMP; ! p. 274) mainly antagonize those of
and kept ready for mobilization (via glucagon) insulin. Glucagon maintains a normal blood
during the interdigestive phase. This provides glucose level between meals and during phases
Hormones and Reproduction bolism). In addition, it promotes growth, inhib- and (b) by stimulating gluconeogenesis from
of increased glucose consumption to ensure a
a relatively constant supply of glucose for the
constant energy supply. It does this (a) by in-
glucose-dependent CNS and vital organs in ab-
sence of food ingestion. Insulin increases the
creasing glycogenolysis (in liver not muscle)
storage of amino acids (AA) in the form of pro-
lactate, AA (protein degradation = catabolism)
teins, especially in the skeletal muscles (ana-
and glycerol (from lipolysis).
its extrahepatic lipolysis (! p. 257, D) and af-
Increased plasma concentrations of amino acids
+
fects K distribution (! p. 180).
(AA) stimulate insulin secretion which would lead to
hypoglycemia without the simultaneous ingestion of
tion is too high. Glucose levels of ! 2 mmol/L
however, since AA also stimulate the release of
(35 mg/dL) produce glucose deficiencies in the brain,
glucagon, which increases the blood glucose con-
which can lead to coma and hypoglycemic shock.
11 Hypoglycemia develops when the insulin concentra- glucose. Hypoglycemia normally does not occur,
centration. Glucagon also stimulates gluconeogene-
The excessive intake of carbohydrates can over-
load glycogen stores. The liver therefore starts to sis from AA, so some of the AA are used for energy
convert glucose into fatty acids, which are trans- production. In order to increase protein levels in
ported to and stored in fatty tissues in the form of tri- patients, glucose must therefore be administered
acylglycerols (! p. 257 D). simultaneously with therapeutic doses of AA to pre-
Diabetes mellitus (DM). One type of DM is in- vent their metabolic degradation.
sulin-dependent diabetes mellitus (IDDM), or type 1
DM, which is caused by an insulin deficiency. Another Somatostatin (SIH). Like insulin, SIH stored in
type is non-insulin-dependent DM (NIDDM), or type 2 D cells (SIH 14 has 14 AA) is released in re-
DM, which is caused by the decreased efficacy of in- sponse to increased plasma concentrations of
sulin and sometimes occurs even in conjunction with glucose and arginine (i.e., after a meal).
increased insulin concentrations. DM is characterized Through paracrine pathways (via G i-linked re-
by an abnormally high plasma glucose concentration ceptors), SIH inhibits the release of insulin
(hyperglycemia), which leads to glucosuria (! p. 158). (! p. 273, B). Therefore, SIH inhibits not only
Large quantities of fatty acids are liberated since the release of gastrin, which promotes diges-
lipolysis is no longer inhibited (! p. 257 D). The fatty tion (! p. 243, B3), but also interrupts the in-
acids can be used to produce energy via acetyl-
coenzyme A (acetyl-CoA); however, this leads to the sulin-related storage of nutrients. SIH also in-
formation of acetoacetic acid, acetone (ketosis), and hibits glucagon secretion (! p. 273 B). This ef-
!-oxybutyric acid (metabolic acidosis, ! p. 142). Be- fect does not occur in the presence of a glucose
cause hepatic fat synthesis is insulin-independent deficiency because of the release of cate-
and since so many fatty acids are available, the liver cholamines that decrease SIH secretion.
begins to store triacylglycerols, resulting in the Somatotropin (STH) = growth hormone
development of fatty liver. (GH). The short-term effects of GH are similar
to those of insulin; its action is mediated by so-
Glucagon, Somatostatin and Somatotropin
Glucagon released from A cells is a peptide matomedins (! p. 280). In the long-term, GH
hormone (29 AA) derived from proglucagon increases the blood glucose concentration and
promotes growth.
(glicentin). The granules in which glucagon is
The effects of glucocorticoids on carbohy-
stored are secreted by exocytosis. Secretion is drate metabolism are illustrated on plate C and
stimulated by AA from digested proteins (es-
284 explained on p. 296.
pecially alanine and arginine) as well as by hy-
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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