(M) Lec 2: Carbohydrates Flashcards
The primary source of energy for the brain, erythrocytes, and retinol cells
Carbohydrates
The major food source and energy supply of the body as the cells depend on this
Carbohydrates
The general empirical formula “Cn(H2O)m” corresponds to what type of carbohydrate?
Monosaccharides
Note: Has the same proportion of H and O with that of water
Carbohydrates have been described as the “what” of carbon?
Hydrates
Depending on the location of the carbonyl functional group, carbohydrates are hydrates of the derivatives of what 2 functional groups?
Aldehydes and Ketones
Carbohydrates are indicated by what shorthand designation?
“CHO”
What 2 functional groups are carbohydrates made out of?
- Carbonyl (C=O)
- Hydroxyl (OH)
This is known as the simplest carbohydrate
Glycoaldehyde
Structures of carbohydrates can be depicted in 2 ways which are?
- Long-chain structure (Fischer projection)
- Ring structure (Haworth projection)
What are the 4 functions of carbohydrates?
- Energy
- Storage
- Structure
- Molecular Recognition
Acronym: M-E-S-S
Classification of Carbohydrates based on the Number of Sugar Units
- Has one sugar unit (simple sugar unit)
- e.g. Glucose, Fructose, and Galactose
Monosaccharides
Classification of Carbohydrates based on the Number of Sugar Units
- Has 2 sugar units or 2 monosaccharides
- Requires being split up by intestinal enzymes so they can be absorbed
- e.g. Sucrose, Lactose, and Maltose
Disaccharides
Classification of Carbohydrates based on the Number of Sugar Units
- Is made up of 2-10 sugar units
Oligosaccharides
Classification of Carbohydrates based on the Number of Sugar Units
- Made up of more than 10 sugar units
Polysaccharides
What is the DISACCHARIDE?
Galactose + Glucose
Lactose
What is the DISACCHARIDE?
Glucose + Glucose
Maltose
What is the DISACCHARIDE?
Glucose + Fructose
Sucrose
Classification of Carbohydrates based on the Size of the Base Carbon
5 carbons
Pentose
Classification of Carbohydrates based on the Size of the Base Carbon
3 carbons
Triose
Classification of Carbohydrates based on the Size of the Base Carbon
6 carbons
Hexose
Classification of Carbohydrates based on the Carbonyl Location
Located on the TERMINAL end
Aldose
Classification of Carbohydrates based on the Carbonyl Location
Located on the middle (usually lands on C2)
Ketose
Reducing or Non-reducing Sugar?
- A double bond is present
- Can donate a free aldehyde or the ketone can be oxidized
- e.g. Glucose, Maltose, Fructose, Lactose, and Galactose
Reducing Sugar
Reducing or Non-reducing Sugar?
- There is no active ketone or aldehyde to be oxidized
- e.g. Sucrose
Non-Reducing Sugar
The sugar present in fruits
Fructose
The sugar present in milk or in mammals
Lactose
Aside from lactose, this sugar is also present in milk
Galactose
The sugar known as “table sugar”
Sucrose
This is the only carbohydrate that is directly used as energy/converted to glycogen for storage
Glucose
What happens to glycogen when the body needs energy?
Converts back to glucose
Digestion of Carbohydrates
Carbohydrates are ingested as what 2 commonly ingested polysaccharides?
Starch and Glycogen
Digestion of Carbohydrates
This enzyme hydrolyzes starch to convert it into disaccharides in the duodenum
Amylase
Digestion of Carbohydrates
This type of amylase is present in the oral cavity
Salivary amylase
Digestion of Carbohydrates
This type of amylase is present in the pancreas
Pancreatic amylase
Digestion of Carbohydrates
After amylase hydrolyzes starch, it will be converted into what 2 products?
Dextrin and Disaccharide
Digestion of Carbohydrates
The acidic pH of the stomach deactivates what enzyme?
Salivary amylase
Digestion of Carbohydrates
When passing through the pancreas, this enzyme will act on the disaccharides to produce another set of disaccharides
Pancreatic amylase
Digestion of Carbohydrates
Where are disaccharides further digested into monosaccharides through the enzymes: maltase, sucrase, or lactase?
Intestines
Digestion of Carbohydrates
Identify the enzyme that breaks these substances apart:
Maltose to 2 glucose units
Maltase
Digestion of Carbohydrates
Identify the enzyme that breaks these substances apart:
Sucrose to glucose and fructose
Sucrase
Digestion of Carbohydrates
Identify the enzyme that breaks these substances apart:
Lactose to glucose and galactose
Lactase
Digestion of Carbohydrates
What form of carbohydrates can be absorbed by the GIT before going to the liver where it will be circulated to the body?
Monosaccharides
These 3 pathways: PPP/HMP, EMP, and TCA, convert glucose into what?
Water and Carbon Dioxide
Aside from water and CO2, these 3 pathways: PPP/HMP, EMP, and TCA, convert glucose into what?
ADP and ATP
Glucose Metabolism
First step for all three pathways: Glucose, with the help of ATP, is coverted into what?
Glucose-6-phosphate (G6P)
Glucose Metabolism
These 2 pathways generate ATP from glucose
- EMP
- HMP
Glucose Metabolism
This pathway allows for the storage of glucose in the form of glycogen which usually occurs in the liver or muscles specialized in storing glycogen
Glycogenesis Pathway
Glucose Metabolism
In case the body needs glucose, what will the liver synthesize in order to convert glycogen into glucose?
Glucose-6-phosphatase (enzyme for G6P)
Glucose Metabolism
Only the liver is capable of synthesizing glucose-6-phosphatase in order to convert glycogen into glucose, what is its equivalent for the muscle if it cannot release the enzyme?
It directly releases glucose via muscle catabolism
Embden-Meyerhoff Pathway
Step 1: Glucose through the action of glucokinase is converted into what?
Glucose-6-phoshate (G6P)
Embden-Meyerhoff Pathway
Step 2: Glucose-6-phoshate (G6P) is converted into what?
pathway to glycogenesis
Glucose-1-phosphate (G1P)
Embden-Meyerhoff Pathway
Step 3: Glucose-1-phosphate (G1P) through the action of glycogen synthase is converted into?
Glycogen
Embden-Meyerhoff Pathway
Optional step: If glycogen is acted upon by glycogen phosphorylase, it will be converted back to what?
Glucose-1-phosphate (G1P)
This becomes glucose again later on
Embden-Meyerhoff Pathway
Step 4: Glucose-6-phosphate may also be converted to become what?
EMP
Clue: Another form of sugar
Fructose-6-phosphate
Embden-Meyerhoff Pathway
Step 5: Fructose-6-phosphate will be converted into what?
Phosphoenol pyruvate (PEP)
Embden-Meterhoff Pathway
Step 6: Phosphoenol pyruvate (PEP) through the action of pyruvate kinase will be converted to?
Pyruvate
Embden-Meyerhoff Pathway
Step 7: Pyruvate will be converted into what before entering the Tricarboxylic Acid Cycle (TCA)?
Acetyl CoA
Other Pathways involving Carbs
Conversion of glucose to pyruvate or lactate
Glycolysis
Other Pathways involving Carbs
Formation of glucose from non-carb sources (e.g. lipids and amino acids)
Gluconeogenesis
Other Pathways involving Carbs
From glycogen to glucose
Glycogenolysis
Other Pathways involving Carbs
From glucose to glycogen
Glycogenesis
Other Pathways involving Carbs
From carbs to fats
Lipogenesis
Other Pathways involving Carbs
The decomposition of fats
Lipolysis
This cycle enables the production of glucose from amino acids, glycogen, glycerol, lactic acid/lactate, or ketone bodies
Tricarboxylic Acid/Citric Acid/ Krebs Cycle
For cases of brief fasting, what organ is the source of glucose?
Liver
For cases of longer fasting times that last for more than a day, the body relies on what process?
Gluconeogenesis
What 3 organs regulate carbohydrates?
- Liver
- Pancreas
- Endocrine Glands
What are the 2 major hormones that control blood glucose?
Insulin and Glucagon
This is both an endocrine and exocrine gland
Pancreas
These glands are able to produce hormones
Endocrine glands
These glands are able to produce enzymes
Exocrine glands
What is the exocrine (enzyme) secretion of the pancreas?
Amylase
What are the endocrine (hormones) secretions of the pancreas?
Clue: Remember the Islets of Langerhans
- Insulin
- Glucagon
- Somatostatin
Islets of Langerhans
Alpha cells secrete what?
Glucagon
Islets of Langerhans
Beta cells secrete what?
Insulin
Islets of Langerhans
Delta cells secrete what?
Somatostatin
Islets of Langerhans
Acinar and Duct cells (exocrine glands) produce what?
Amylase
Islets of Langerhans
F cells secrete what?
Pancreatic polypeptides
The most important hormone in the blood glucose concentration; the main hypoglycemic agent
Insulin
The only hormone responsible for the entry of glucose into the cell
Insulin
TOF: Insulin decreases the process of glycogenesis, lipogenesis, and glycolysis BUT increases glycogenolysis hence why it is a hypoglycemic agent
False (reverse the decrease and increase portions)
Insulin is released when blood glucose levels are what?
High
Stimulates the entrance of glucose into tissue (decreases blood sugar)
This is released during stressed and fasting stages; the main hyperglycemic agent
Glucagon
This hormone increases the processes of glycogenolysis and gluconeogenesis
Glucagon
Once insulin is released, the glucose in the blood goes to where?
Body cells (or muscles)
TOF: Insulin production rates increase when glucose is absorbed by the muscles
False (because glucose is now in your body cells, not your blood, so there is nothing for insulin to counter)
Insulin can stimulate what organ to take up glucose and store it as glycogen?
Liver
Once glucagon is released in the blood, it stimulates the liver to break down what to become glucose?
Glycogen
This is produced by the medulla of the adrenal glands (specifically chromaffin cells); it inhibits insulin making it a hyperglycemic agent as it increases the processes of glycogenolysis and lipolysis
Catecholamines
TOF: Catecholamines are released with stress
True
This is produced by the adrenal cortex (zona fasciculata and zona reticularis); it decreases glucose entry into the cell which increases the processes of gluconeogenesis, lipolysis, and glycogenolysis
Glucocorticoids
This is the main promoter of gluconeogenesis in glucocorticoids
Cortisol (hyperglycemic hormone)
Glucocorticoids are made up of what 2 substances?
Cortisol and Corticosteroids
Hyperglycemic Hormones
Aka “somatotropic hormone” which causes decreased entry of glucose to cells
Growth hormone
Hyperglycemic Hormones
Increases blood glucose by stimulating the release of cortisol from the adrenal glands
ACTH
Hyperglycemic Hormones
A thyroid hormone that promotes glycogenolysis and gluconeogenesis (+ intestinal absorption of glucose)
Thyroxine
Hyperglycemic Hormones
A hormone-inhibiting hormone
Somatostatin
Clinical Conditions of Carbohydrate Metabolism
An increase in blood or plasma glucose levels
Hyperglycemia
Clinical Conditions of Carbohydrate Metabolism
TOF: Insulin deficiency directly results to hyperglycemia
True
Clinical Conditions of Carbohydrate Metabolism
A lack of this receptor prevents the passing of insulin through the cells which prevents the glucose from entering the cells, contributing to hyperglycemia
Insulin receptor
Clinical Conditions of Carbohydrate Metabolism
With hyperglycemia, all adults older than how many years old should have their FBS checked every 3 years unless diabetic?
45 years old
Clinical Conditions of Carbohydrate Metabolism
TOF: Ketones are decreased in the serum and urine when a patient is hyperglycemic
False (increased)
Clinical Conditions of Carbohydrate Metabolism
Why is blood and urine pH decreased when the patient is experiencing hyperglycemia? What urinary tract event is experienced when blood glucose levels are high?
Polyuria = decreases urine pH
Clinical Conditions of Carbohydrate Metabolism
A decrease in blood or plasma glucose levels which is usually a warning sign for CNS-related disorders
Hypoglycemia
Clinical Conditions of Carbohydrate Metabolism
What is the characteristic sign and symptom of hypoglycemia?
Whipple’s Triad
- Hypoglycemic symptoms
- Low blood glucose concentration
- Immediate relief after glucose administration
Clinical Conditions of Carbohydrate Metabolism
TOF: The Whipple’s Triad is used to diagnose patients that have diabetes
False (no diabetes)
Hypoglycemia
Clinical Conditions of Carbohydrate Metabolism
What glucose level indicates that glucagon and other hyperglycemic hormones are being released by the endocrine gland?
65 to 70 mg/dL
Clinical Conditions of Carbohydrate Metabolism
Hypoglycemia symptoms are observable at what glucose level?
50-55 mg/dL
Clinical Conditions of Carbohydrate Metabolism
What is the diagnostic glucose level for hypoglycemia?
Less than 50 mg/dL
Classifications of Hypoglycemia can be Based on:
“Whether administered with insulin, alcohol, or salicylates”
A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia
A. Drug Administration
Classifications of Hypoglycemia can be Based on:
“Those with hepatic failure, renal failure, or sepsis”
A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia
B. Critical Illnesses
Classifications of Hypoglycemia can be Based on:
“Deficiency of GH or cortisol deficiency”
A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia
C. Hormonal Deficiency
Classifications of Hypoglycemia can be Based on:
“Wherein there is a pancreatic beta cell disorder”
A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia
D. Endogenous Hyperinsulinism
Classifications of Hypoglycemia can be Based on:
“There is a production of insulin autoantibodies”
A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia
E. Autoimmune Hypoglycemia
Classifications of Hypoglycemia can be Based on:
“Such as leukemia or hepatoma”
A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia
F. Non-Beta Cell Tumors
Classifications of Hypoglycemia can be Based on:
“Cases of post-gastric surgery”
A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia
H. Alimentary Hypoglycemia
Classifications of Hypoglycemia can be Based on:
“Cause is unknown”
A. Drug Administration
B. Critical Illnesses
C. Hormonal Deficiency
D. Endogenous Hyperinsulinism
E. Autoimmune Hypoglycemia
F. Non-Beta Cell Tumors
G. Hypoglycemia of Infancy and Childhood
H. Alimentary Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia
I. Idiopathic Postprandial Hypoglycemia
A group of metabolic disorders characterized by hyperglycemia
Diabetes Mellitus
This condition is caused by defects in insulin secretion, insulin receptors, or both
Diabetes Mellitus
This is exhibited when the plasma glucose level exceeds 180 mg/dL with a normal renal function
Glucosuria
This condition is also exhibited in Diabetes Mellitus but may be reversed by insulin administration
Ketosis
TOF: Ketone bodies are frequently found in patients with severe uncontrolled diabetes
True
Endocrine disorders such as Cushing’s Syndrome, Acromegaly, or Pheochromocytoma have an increased release of hormones that (increase/decrease) blood glucose levels
Increase
Types of DM:
Aka insulin dependent DM, juvenile onset DM, brittle diabetes, or ketosis-prone diabetes
Type 1
Types of DM:
Caused by the cellular mediated autoimmune destruction of B cells in the pancreas
Type 1
Types of DM:
Manifested by insulinopenia wherein there is absolute insulin deficiency due to the loss of pancreatic B cells which resuts to the dependency in insulin to sustain life and prevent ketosis
Type 1
Types of DM:
There is a genetic association with HLA DR3 and DR4 located on Chromosome 6
Type 1
Types of DM:
There is a presence of multiple autoantibodies (glutamic acid decarboxylase and insulin autoantibodies)
Type 1
Types of DM:
This type is rare, has no known etiology, strongly inherited, no B-cell autoantibodies, episodic insulin requirements, and is prone to developing ketosis
Idiopathic Type 1 DM
Types of DM:
What are the 3 signs and symptoms of type 1 DM?
Clue: 3Ps
- Polyuria
- Polydipsia
- Polyphagia
Types of DM:
Aka non-insulin dependent DM, adult type/maturity onset DM, stable diabetes, ketosis-resistant DM, or receptor-deficient DM
Type 2
Types of DM:
This is a relative-type of insulin deficiency as opposed to the other type with absolute deficiency
Type 2
Types of DM:
This is caused by a resistance to insulin due to a deficiency in insulin receptors
Type 2
Types of DM:
This is a geneticist’s worst nightmare because of its genetic predisposition
Type 2
Types of DM:
Results to non-ketotic hyperosmolar coma (overpopulation of glucose) plus a notable increase in BUN and creatinine
Type 2
Types of DM:
This type has no presence of ketoacidosis
Type 2
Types of DM:
In this type, insulin is present but there is no receptor that is why the C-peptide is linked to be present (C-peptide is produced with insulin)
Type 2
Types of DM:
What are the 3 signs and symptoms of Type 2 DM?
Clue: 3Ps
- Polyuria
- Polydipsia
- Polyphagia
This is characterized by a deficiency in ADH or vasopressin with normoglycemia, severe polyuria, and polydipsia (decreased SG but increased urine volume)
Diabetes Insipidus
Diabetes Mellitus Table (Type 1 or 2)
Incidence Rate: 10-15%
Type 1
Diabetes Mellitus Table (Type 1 or 2)
Incidence Rate: 90-95%
Type 2
Diabetes Mellitus Table (Type 1 or 2)
Onset: Any (childhood/teens)
Type 1
Diabetes Mellitus Table (Type 1 or 2)
Onset: Over 40 years old
Type 2
Diabetes Mellitus Table (Type 1 or 2)
Risk Factors: Genetic/Autoimmune
Type 1
Diabetes Mellitus Table (Type 1 or 2)
Risk Factors: Genetics, obesity, and lifestyle
Type 2
Diabetes Mellitus Table (Type 1 or 2)
C-Peptide Levels: Decreased or undetectable
Type 1
Diabetes Mellitus Table (Type 1 or 2)
C-Peptide Levels: Detectable
Type 2
Diabetes Mellitus Table (Type 1 or 2)
Pre-diabetes: (+) for autoantibodies
Type 1
Diabetes Mellitus Table (Type 1 or 2)
Pre-diabetes: (-) for autoantibodies
Type 2
Diabetes Mellitus Table (Type 1 or 2)
Symptomatology: Symptoms develop abruptly
Type 1
Diabetes Mellitus Table (Type 1 or 2)
Symptomatology: Symptoms develop gradually (some are asymptomatic)
Type 2
Diabetes Mellitus Table (Type 1 or 2)
Ketosis: Common and poorly controlled
Type 1
Diabetes Mellitus Table (Type 1 or 2)
Ketosis: Rare
Type 2
Diabetes Mellitus Table (Type 1 or 2)
Medication: Insulin absolute
Type 1
Diabetes Mellitus Table (Type 1 or 2)
Medication: Oral agents
Type 2
TOF: Genetic syndromes such as Down’s syndrome or Klinefelter syndrome can also have an increased chance to manifest diabetes mellitus
True
