Hypoglycemia

Tevin Erlambang and Chelsea Taylor

BIOL 3410 1: Biochemistry
Term Paper
April 20, 2016
Dr. Ratna Gupta
Our Lady of the Lake College

Hypoglycemia, as its names implies, hypo- meaning low and glycemia meaning sugar,
is a condition of low blood sugar or low blood glucose. Essentially this condition occurs when
the levels of glucose in the blood drop below normal. It can occur frequently occur in type 1 and
type 2 diabetics (Ensling, Steinmann, & Whaley-Connell, 2011). This condition is important to
note because in mammals glucose serves as a source of energy. Glucose is the only fuel that the
brain uses under non-starvation conditions and the only fuels that red blood cells can use at all
(Tymoczko, Berg, & Stryer, 2010).
There are several causes of hypoglycemia. These causes of hypoglycemia can be split
into a few main groups: Endocrine, Metabolic, Other, and Idiopathic. Endocrine causes of
hypoglycemia include hyperinsulinism, adrenal insufficiency, hypopituitarism, growth hormone
deficiency, and hypothyroidism (Bonham, Reed, Lang, & Losty, 2011). Other causes of
hypoglycemia include neonatal complications, drug related, and liver failure (Bonham et al.,
2011). Idiopathic ketotic hypoglycemia is a common cause of hypoglycemia in children.
Metabolic causes of hypoglycemia include disorders of: fatty acid oxidation and carnitine
transport, carbohydrate metabolism, organic acid metabolism, and gluconeogenesis (Bonham et
al., 2011).
There are a two main categories of hypoglycemia: diabetic and non-diabetic. Diabetic
hypoglycemia occurs when a person with diabetes, a condition of hyperglycemia or increased
blood glucose levels, have too low levels of blood sugar. This is generally caused by antidiabetic
medications that they may be taking. Non-diabetic hypoglycemia occurs when a person with no
history or diagnosis of diabetes experiences periodic spells of hypoglycemia
(Hypoglycemia.co.uk, 2016). There are other types of hypoglycemia that describe when the

periods of hypoglycemia occur. These other types of non-diabetic hypoglycemia include: fasting
hypoglycemia, ketotic hypoglycemia, and reactive hypoglycemia (Hypoglycemia.co.uk, 2016).
Examples of common symptoms seen in hypoglycemia include: hunger, fatigue,
shakiness, nervousness, confusion, sweating, dizziness, difficulty speaking, anxiety, and
weakness (Fonseca, Martin, & White, 2008). Severe hypoglycemia occurs when hypoglycemia is
not treated. Symptoms of severe hypoglycemia can include convulsions and loss of
consciousness. In its most serious form, hypoglycemia can result in coma or even death.
The theory behind hypoglycemia is an over -response or lack of a response from one or
more hormones. Everyone needs to have a certain amount of sugar in their blood to survive.
Blood sugar is needed to allow our muscles and organs, including our heart and brain, to
function. Too much or too little glucose in the blood can cause problems for the body in the short
term and in the long term.
In order for the bodys cells to receive energy there needs to be sufficient glucose in the
blood to feed the cells with. In addition, the hormone insulin is needed to help transport glucose
from the blood into cells. When glucose is transported from the blood into the cells, this results
in a decrease in our blood sugar levels. The pancreas will respond to rises in blood sugar by
releasing an appropriate level of insulin to transport the right amount of glucose from the blood
into cells. If the body produces, or is given, too much insulin then too much glucose will be
taken from the blood and blood glucose levels will drop too low.
When blood glucose concentration declines, the alpha cells of the pancreas secrete
glucagon. Glucagon works by stimulating the liver to release glucose into the blood which can

restore blood sugar back to normal levels. The effects of glucagon to return blood glucose to
normal depends upon the location. In the liver and skeletal muscle, glucagon causes an increased
breakdown of glycogen to glucose. In adipose or fatty tissue, glucagon causes an increased
breakdown of fats to fatty acids. In the liver alone, glucagon causes the increased synthesis and
release of glucose. All of these mechanisms are an attempt for the pancreas to make the blood
glucose concentration rise back to normal. The normal state of blood glucose is called glucose
homeostasis.
Glucose is so important to the body that it uses several pathways and transporters to
attempt to maintain homeostasis. Glucose pathways include: glycolysis and gluconeogenesis.
Glycolysis is an energy-conversion pathway that converts glucose into pyruvate; pyruvate can
then be converted into energy. Gluconeogenesis is the synthesis of glucose from noncarbohydrate precursors. It converts pyruvate into glucose. Gluconeogenesis in the liver and
kidney helps to maintain the glucose concentration in the blood, from which it can be extracted
by the brain and muscle to meet their metabolic demands (Tymoczko et al., 2010). The balance
between glycolysis and gluconeogenesis is sensitive to blood-glucose concentration.
The glucose family of transporters includes five transporters, each with a distinctive role.
They are respectively name GLUT1 GLUT5. GLUT 1 and GLUT 3 are present in all
mammalian tissues. Under normal conditions, they are responsible for transporting glucose into
the cell at a constant rate (Tymoczko et al., 2010). GLUT 2 is present in liver and pancreatic beta
cells. The pancreas senses the level of glucose in the blood and adjusts the rate of insulin
secretion. Insulin signals the need to remove glucose from the blood for storage as glycogen or
conversion into fat. Glucose rapidly enter the liver cells only in times of high glucose in the

blood (Tymoczko et al., 2010). GLUT 4 transports glucose into muscle and fat cells. In the
presence of insulin, GLUT4 transporters in the plasma membrane increase. This promotes insulin
uptake of glucose by muscle and fat (Tymoczko et al., 2010). GLUT5 is present in the small
intestine. It functions as a transporter for fructose (Tymoczko et al., 2010).
Glycogen is a storage form of glucose that can be readily broken down to yield glucose
molecules when energy is needed. Glycogen is synthesized and degraded by different pathways.
Glycogen pathways include: glycogenesis and glycogenolysis.
Glycogenesis is an anabolic process which requires ATP energy to store excess glucose
molecules into more complex glycogen granules. Glycogen is synthesized primarily by
hepatocytes and muscle. Glycogenesis is initiated by the anabolic hormone insulin. Digestion of
food yields glucose which is transported from the gut to the circulating blood: Elevated plasma
glucose causes the pancreatic beta cells to release insulin and Increased plasma insulin activates
anabolic pathways in the liver, muscle, fat, kidney and brain. These organs react by: facilitating
GLUT synthesis, expression and diffusion of glucose into the cell, increasing glucose
metabolism, enhancing the storage of excess glucose, inhibiting the catabolic release of glucose
by suppressing the action of glucagon, enhancing lipid production. All of these activities have the
effect of reducing excess plasma glucose
Glycogenolysis is a catabolic process that breaks down stored glycogen into glucose.
Glycogenolysis provides glucose during short periods of fasting, between meals, during sleep,
etc. Glucagon produced in the pancreatic alpha cell and the adrenal catecholamines epinephrine
and norepinephrine are the catabolic hormones that regulate glycogenolysis. Glucagon and
catecholamines activate the enzyme glycogen phosphorylase. Glycogen phosphorylase breaks

the bonds holding individual glucose molecules to the glycogen macromolecules, stored in
hepatocytes and myocytes. The liver and muscle are the primary targets of glucagon induced
glycogenolysis. Liver and muscle are capable of absorbing large quantities of glucose and storing
it as glycogen in response to insulin.
Glycolysis Helps Pancreatic Beta Cells Sense Glucose. Insulin is secreted by cells of
the pancreas in response to high blood levels of glucose. This secretion is stimulated by the
metabolism of glucose by the cells. Insulin release is regulated by ATP. The metabolism of
glucose by glycolysis increases the concentration of ATP, which causes an ATP-sensitive
potassium channel to close. The closure of this channel alters the charge across the membrane
() and causes a calcium channel to open.

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