Ingles Medicina Parrafo 1

In view of the obligatc glucose requirements of the central nervous systcm,
prevention of a low plasma glucose concentration (hypoglycemia) is critical

to survival. Normally the plasma glucose concentration is maintained within
narrow limits by a tightly regulated balance between glucose efflux from and
influx into the circulation. Moreover, entry of glucose from ingested
carbohydrate normally is intermiltent; the postprandial period is a state
enhanced glucose metabolism and storage and
suppreSsed endogenous glucose production. In contrast, the poslabsorptive
period is a state of partially suppressed glucose utilization and enhanced
glucose production. The latter is the result of the breakdown of glycogen
(glycogenolysis) and the formation of new glucose (gluconeogenesis). Under
most circumstances the liver is the predominant source of endogenous
glucose production, although the kidneys become a major source of glucose
during prolonged fasting. After an overnight fast most endogenous
glucose production is from glycogenolysis, but after approxilhately 24 hours
of fasting virtually all the glucose produced is by gluconeo genesis.
The prevention of hypoglycemia between meals requires structurally and

enzymatically intacl liver, adequate hepatic glycogen stores and an adequate
supply of gluconeogenic precursors (lactatc, pyruvate, glycerol, and
gluconcogenic amino acids such as alanine); and appropriate regulatory
signals.
The major regulatory signals involved in transition between the fed and the
fasted state are insulin and glucagón. Insulin secreted from pancreatic beta
cells into the portal circulation in response to a meal, suppresses hepatic
glucose production and stimulates glucose utilization by insulin-sensitive
tissues. Glucagon stimulates hepatic glucose production by both
glycogenolysis and gluconcogenesis. Its secretion from pancreatic alpha cells
is suppressed after a carbohydrate meal which favors glucose conservation.
In the postabsorptivea state, insulin secretion is suppressed and glucagón
secretion increases.
This combination of low insulin and high glucagón hormonal signals resuts in
accelerated hepatic glucose production and diminished glucose utilitation, In
addition to glucagón , the hormone ephinephine, cortisol, and growth
hormone also promote glucose production and limit glucose utilization.
Glucagón, epinephrine, cortisol, and growth hoemone are often referred to
as glucose counterregulatory hormones.
Physiologic studies have shown that the following principles (summarized

in Fig. 304- l) govern glucose counterregulation and the prevention or
correction of hypoglycemia:
l. Decreased insulin secretion plays an important role in prevention or
correction or hypoglycemia. However, glucose counterregulation is not due
solely to dissipation of insulin but rather to coordinated dissipation of insulin
and activation of redundant glucose counterregulatory systems.
2. Glucagon plays a primary counterrcgulatory role.
3. Epinephrine is not normally required for glucose counterregulation but
compensates to a large degree when glucagon secretion is deficient (e.g.,
during insulin-induced hypoglycemia in type I diabetes mellitus).
Hypoglycemia occurs or progresses only when both glucagon and
epinephrine are deficient and insulin is present, or when insulin action is
excessive.
4. Cortisol and growth hormone are not critical to correction of
hypoglycemia or to prevention of hypoglycemia after an ovemight fast.
Nevertheless, patients with chronic deficiencies of these hormones
occasionally develop fasting hypoglycemia.
5. Although other hormones, neural mechanisms, or glucose

autoregulation may be involved in counterregulation, they are not
sufficicnlly potent to prevent or conect hypoglycemia when both
glucagon and epinephrine are deficient and insulin is present.
The glycemic threshold for suppression of insulin secretion in response to

declining plasma glucose level lies well within the physiologic range for
plasma glucose. In keeping withi their role in prevention as well as
correction of hypoglyccmia, the glycemic thresholds for relcase of
counterregulatory hormones lie just below the physiologic plasma glucose
range and well above the threshold for symptoms of hypoglyccmia.

Ingles Medicina Parrafo 1

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Ingles Medicina Parrafo 1

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In view of the obligatc glucose requirements of the central nervous systcm,

prevention of a low plasma glucose concentration (hypoglycemia) is critical

The prevention of hypoglycemia between meals requires structurally and

Physiologic studies have shown that the following principles (summarized

5. Although other hormones, neural mechanisms, or glucose

The glycemic threshold for suppression of insulin secretion in response to

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