Glucose

Homeostasis
Evaluation

Brenda Phang Joo Yee

124202

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WHY???

WHY???

Glucose homeostasis

Fasting /
Postabsorptive
state

quasi-equilibrium situation
occurring after a 12- to 16-hour
overnight fast

Dynamic
postprandial
state
persists for up to 6
hours after meal
ingestion

Recently, considerable attention has been focused on the

postprandial state.
WHY???
because isolated postprandial hyperglycemia, as occurs in people
with impaired glucose tolerance, has been shown to double the
risk for death from cardiovascular disease and because
postprandial hyperglycemia appears to be the rate-limiting
factor for achieving optimal glycemic control in patients with

The postprandial state: 4-h period that immediately follows

ingestion of a meal. During this period, dietary
carbohydrates are progressively hydrolyzed through several
sequential enzymatic actions. Even though the insulin
response rapidly reduces the postprandial glucose excursion
with a return to baseline levels within <2 h, the overall
period of absorption has approximately a 4-h duration that
corresponds to the postprandial state.

The postabsorptive state consists of a 6-h period that

follows the postprandial period. During this time interval,
glucose concentrations remain within a normal range in
nondiabetic individuals through the breakdown of the
glycogen (glycogenolysis) stored during the postprandial
period.

The real fasting state commences only at the end of the

postabsorptive period (1012 h after the beginning of the
last meal intake).

lationship btwn plasma glucose and insulin secreti

Two phases of insulin secretion

following a glucose load.
1. Initial phase: reflects secretion
of preformed insulin
2. secondary rise is due to
secretion of newly synthesised
insulin.

The rate of insulin

secretion as a function of
the plasma glucose
concentration.

Nondiabetic individuals:
- approximately 50% of the total daily insulin is secreted
during basal periods (suppressing lipolysis, proteolysis,
and glycogenolysis)
- The remainder of insulin secretion is postprandial.

In response to a meal, there is a rapid and sizable

release of preformed insulin from storage granules
within the beta cell. This "first phase" of insulin secretion
promotes peripheral utilization of the prandial nutrient
load, suppresses hepatic glucose production, and
limits postprandial glucose elevation.

First-phase insulin secretion: begins within 2 minutes of

nutrient ingestion and continues for 10 to 15 minutes.

The second phase of prandial insulin secretion follows, and

is sustained until normoglycemia is restored.

Figure: Schematic
illustration of the plasma
insulin response to a
hyperglycaemic clamp,
showing gradual
decrease in first phase as
well as second phase
insulin secretion as
glucose tolerance
deteriorates from normal
to impaired and further
to mild and advanced
diabetes.

Fed State

Insulin-sensitive
tissues:
responsible for
70% of
postprandial
glucose clearance
Glucose Uptake by Insulin-Sensitive Tissues

disposal after meal ingestion in individuals with normal

Postprandial
glucose disposal =
the sum of
splanchnic and
peripheral tissue
glucose uptake
It may seem surprising that
brain plays a substantial role
because its uptake of glucose is
generally considered to be
insulin independent. But
because after meal ingestion
its use of glucose remains
constant while the supply of
endogenous glucose decreases,
the brain's requirement for
glucose must be met by
glucose from the meal.

Since brain does not store

glucose, its uptake of glucose
should be destined wholly for
glycolysis (and oxidation)

muscle, brain, and kidney

2/3
BRAIN - 65%
MUSCLE &
OTHERS - 35%

LIVER
(first-pass extraction
from the portal vein
as well as uptake via
the hepatic artery)

1/3
LIVER - 60%
MUSCLE - 40%

Normal - during postprandial state/fed state - high

glucose activates insulin secretion - glucose
uptake by insulin sensitive tissues (70%) & noninsulin sensitive tissues (30%) occur gluconeogenesis + glycogenolysis inhibited maintain normal blood glucose level.

IGT patient - abnormal postprandial glucose why???

insulin is very crucial for insulin sensitive tissues as they determines plasma glucose level (70% of
uptake) - slight decrease in insulin function will
cause increase in blood glucose level

Postprandial Hyperglycemia

Fasting State
Glucagon-Mediated Hepatic Glucose Output

In the fasting/post-absorptive state:

- the majority (7075%) of glucose uptake occurs
in insulin-insensitive tissues (brain, erythrocytes,
and splanchnic tissues)
- only 25% of glucose uptake occurring in insulinsensitive tissues.
- total body glucose uptake is precisely matched by
the rate of endogenous glucose production,
primarily by the liver and to a smaller extent by the
kidney

Normal - during fasting - glucagon activated - gluconeogenesis

+ glycogenolysis occur - will increase plasma glucose level - but
glucose uptake by insulin insensitive tissues & insulins counter
regulatory effect that suppress the enormous effect of glucagon
- to maintain normal blood glucose level.

IGT patient - normal fasting glucose - why???

insulin level is still near normal, the slight insulin effect can
counter with high glucagon level, to suppress some effect of
glucagon in causing high blood glucose level

DM patient - abnormal fasting glucose - why???

insulin resistance occur - low/near absence of insulin effect cant counter regulate glucagons activity - gluconeogenesis and
glycogenolysis overstimulated - hyperglycaemia

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