CENTRAL LUZON DOCTOR’S HOSPITAL - EDUCATIONAL INSTITUTION

SAN PABLO, TARLAC CITY

Carbohydrate Metabolism
Group 3
 Table of Contents

I. Objective……………………………………………………………… I

II. Introduction…………………………………………………………... II

III. Body………………………………………………………………….. III

IV. Case Study……………………………………………………………. IV

V. Reference……………………………………………………………. V
 Objective
Describe the metabolism and digestion of Carbohydrate. Disease connected to problems with
carbohydrate metabolism.
 Introduction

Carbohydrate metabolism is the whole of biochemical processes responsible for the metabolic

formation, breakdown, and interconversion of carbohydrates in living organisms.

Carbohydrates are central to many essential metabolic pathways. Plants synthesize carbohydrates

from carbon dioxide and water through photosynthesis, allowing them to store energy absorbed

from sunlight internally. When animals and fungi consume plants, they use cellular respiration to

break down these stored carbohydrates to make energy available to cells. Both animals and

plants temporarily store the released energy in the form of high energy molecules, such as ATP,

for use in various cellular processes.

Although humans consume a variety of carbohydrates, digestion breaks down complex

carbohydrates into a few simple monomers (monosaccharides) for metabolism: glucose, fructose,

and galactose. Glucose constitutes about 80% of the products, and is the primary structure that is

distributed to cells in the tissues, where it is broken down or stored as glycogen. In aerobic

respiration, the main form of cellular respiration used by humans, glucose and oxygen are

metabolized to release energy, with carbon dioxide and water as byproducts. Most of the fructose

and galactose travel to the liver, where they can be converted to glucose.

Some simple carbohydrates have their own enzymatic oxidation pathways, as do only a few of

the more complex carbohydrates. The disaccharide lactose, for instance, requires the enzyme

lactase to be broken into its monosaccharide components, glucose and galactose.

 BODY

Glycolysis

Glycolysis is the process of breaking down a glucose molecule into two pyruvate molecules,
while storing energy released during this process as ATP and NADH. Nearly all organisms that
break down glucose utilize glycolysis. Glucose regulation and product use are the primary
categories in which these pathways differ between organisms. In some tissues and organisms,
glycolysis is the sole method of energy production. This pathway is common to both anaerobic
and aerobic respiration.

Glycolysis consists of ten steps, split into two phases. During the first phase, it requires the
breakdown of two ATP molecules.[1] During the second phase, chemical energy from the
intermediates is transferred into ATP and NADH. The breakdown of one molecule of glucose
results in two molecules of pyruvate, which can be further oxidized to access more energy in
later processes.

Gluconeogenesis

Gluconeogenesis is the reverse process of glycolysis. It involves the conversion of non-

carbohydrate molecules into glucose. The non-carbohydrate molecules that are converted in this
pathway include pyruvate, lactate, glycerol, alanine, and glutamine. This process occurs when
there are lowered amounts of glucose. The liver is the primary location of gluconeogenesis, but
some also occurs in the kidney.

This pathway is regulated by multiple different molecules. Glucagon, adrenocorticotropic

hormone, and ATP encourage gluconeogenesis. Gluconeogenesis is inhibited by AMP, ADP,
and insulin.
Glycogenolysis

Glycogenolysis refers to the breakdown of glycogen. In the liver, muscles, and the kidney, this
process occurs to provide glucose when necessary. A single glucose molecule is cleaved from a
branch of glycogen, and is transformed into glucose-1-phosphate during this process. This
molecule can then be converted to glucose-6-phosphate, an intermediate in the glycolysis
pathway.

Glucose-6-phosphate can then progress through glycolysis. Glycolysis only requires the input of
one molecule of ATP when the glucose originates in glycogen. Alternatively, glucose-6-
phosphate can be converted back into glucose in the liver and the kidneys, allowing it to raise
blood glucose levels if necessary.

Glucagon in the liver stimulates glycogenolysis when the blood glucose is lowered, known as
hypoglycemia. The glycogen in the liver can function as a backup source of glucose between
meals. Adrenaline stimulates the breakdown of glycogen in the skeletal muscle during exercise.
In the muscles, glycogen ensures a rapidly accessible energy source for movement.

Glycogenesis

Glycogenesis refers to the process of synthesizing glycogen. In humans, excess glucose is

converted to glycogen via this process. Glycogen is a highly branched structure, consisting of
glucose, in the form of glucose-6-phosphate, linked together. The branching of glycogen
increases its solubility, and allows for a higher number of glucose molecules to be accessible for
breakdown. Glycogenesis occurs primarily in the liver, skeletal muscles, and kidney.

Pentose phosphate pathway

The pentose phosphate pathway is an alternative method of oxidizing glucose. It occurs in the
liver, adipose tissue, adrenal cortex, testis, milk glands, phagocyte cells, and red blood cells. It
produces products that are used in other cell processes, while reducing NADP to NADPH. This
pathway is regulated through changes in the activity of glucose-6-phosphate dehydrogenase.
Fructose metabolism

Fructose must undergo certain extra steps in order to enter the glycolysis pathway. Enzymes
located in certain tissues can add a phosphate group to fructose. This phosphorylation creates
fructose-6-phosphate, an intermediate in the glycolysis pathway that can be broken down directly
in those tissues. This pathway occurs in the muscles, adipose tissue, and kidney. In the liver,
enzymes produce fructose-1-phosphate, which enters the glycolysis pathway and is later cleaved
into glyceraldehyde and dihydroxyacetone phosphate.

Galactose metabolism

Lactose, or milk sugar, consists of one molecule of glucose and one molecule of galactose. After
separation from glucose, galactose travels to the liver for conversion to glucose. Galactokinase
uses one molecule of ATP to phosphorylate galactose. The phosphorylated galactose is then
converted to glucose-1-phosphate, and then eventually glucose-6-phosphate, which can be
broken down in glycolysis.
 Lactose Intolerance

Lactose intolerance is a condition in which people have symptoms due to the decreased ability to
digest lactose, a sugar found in dairy products. Those affected vary in the amount of lactose they
can tolerate before symptoms develop. Symptoms may include abdominal pain, bloating,
diarrhea, gas, and nausea. These symptoms typically start thirty minutes to two hours after eating
or drinking milk-based food. Severity typically depends on the amount a person eats or drinks.
Lactose intolerance does not cause damage to the gastrointestinal tract.

Lactose intolerance is due to the lack of enzyme lactase in the small intestines to break lactose
down into glucose and galactose. There are four types: primary, secondary, developmental, and
congenital. Primary lactose intolerance occurs as the amount of lactase declines as people age.
Secondary lactose intolerance is due to injury to the small intestine such as from infection, celiac
disease, inflammatory bowel disease, or other diseases. Developmental lactose intolerance may
occur in premature babies and usually improves over a short period of time. Congenital lactose
intolerance is an extremely rare genetic disorder in which little or no lactase is made from birth.

Signs And Symptoms

The principal symptom of lactose intolerance is an adverse reaction to products containing

lactose (primarily milk), including abdominal bloating and cramps, flatulence, diarrhea, nausea,
borborygmi, and vomiting (particularly in adolescents). These appear one-half to two hours after
consumption. The severity of symptoms typically increases with the amount of lactose
consumed; most lactose-intolerant people can tolerate a certain level of lactose in their diets
without ill effects.
 Causes

Primary hypolactasia, or primary lactase deficiency, is genetic, only affects adults, and is caused
by the absence of a lactase persistence allele. In individuals without the lactase persistence allele,
less lactase is produced by the body over time, leading to hypolactasia in adulthood. The
frequency of lactase persistence, which allows lactose tolerance, varies enormously worldwide,
with the highest prevalence in Northwestern Europe, declines across southern Europe and the
Middle East and is low in Asia and most of Africa, although it is common in pastoralist
populations from Africa.

Secondary hypolactasia or secondary lactase deficiency, also called acquired hypolactasia or

acquired lactase deficiency, is caused by an injury to the small intestine. This form of lactose
intolerance can occur in both infants and lactase persistent adults and is generally reversible. It
may be caused by acute gastroenteritis, coeliac disease, Crohn's disease, ulcerative
colitis,chemotherapy, intestinal parasites (such as giardia), or other environmental causes.

Primary congenital alactasia, also called congenital lactase deficiency, is an extremely rare,
autosomal recessive enzyme defect that prevents lactase expression from birth. People with
congenital lactase deficiency cannot digest lactose from birth, so cannot digest breast milk. This
genetic defect is characterized by a complete lack of lactase (alactasia). About 40 cases have
been reported worldwide, mainly limited to Finland. Before the 20th century, babies born with
congenital lactase deficiency often did not survive, but death rates decreased with soybean-
derived infant formulas and manufactured lactose-free dairy products.

Recommendations

 Milk substitutes
 Lactase supplements
 Rehabituation to dairy products
 Reference

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