cc carbs part 1

carbohydrates

Are compounds containing C, H, and O

C=O(carbonyl) and -OH (hydroxyl groups)

carbohydrates contain:

active aldehyde and ketone group

in order for a certain carbohydrate to be a reducing substance, it should contain an

Glucose

Maltose

Fructose

Lactose

Galactose

examples of carbohydrates

glucose

primary source of energy for the brain, erythrocyte and for the human retinal cells.

trioses

contain three carbons

tetrose

contain 4 carbons

pentoses

contain five carbons

contain 6 carbons

hexoses

aldose

would have a carbonyl group located on the terminal part

ketose

would have a carbonyl group located in the middle and is connected to other carbon atoms

monosaccharides

1 unit of simple sugar that cannot be hydrolyzed into a simpler form

glucose

fructose

galactose

examples of monosaccharides

disaccharides

form from the joining of two carbohydrates molecules or two monosaccharides joined by glycosidic linkage

maltose

lactose

sucrose

examples of disaccharides

glu+glu

composition of maltose

glu+gal

composition of lactose

glu+fru

composition of sucrose

oligosaccarides

contain 2-10 sugar units

raffinose

(1glu+1fru+1gal) = trisaccharide

stachyose

(2gal+1fru+1glu) =tetrassacharide

polysaccharides

contain more that 10 monosaccharides

starch and glycogen

examples of polysaccharides

D series

dextrorotatory (hydroxyl group is located on the right of fisher projection)

/ projected on carbon 5

L series

leverotatory (hydroxyl group is located on the left part of fisher on carbon 5 projection) / projected on carbon 5

polymers

large molecules which are composed of many subunits.

Salivary amylase and pancreatic amylase

are responsible for the digestion of these polymers to dextrins and disaccharides which are further hydrolyzed to monosaccharides by maltase.

maltase

maltose to glucose + glucose

sucrase

sucrose to glucose + fructose

lactase

lactose to glucose + galactose

glucose-6-phosphate; hexokinase

First step of all 3 pathways → glucose is converted to — using high-energy molecule, ATP catalyzed by the enzyme —

• embden-meyerhof pathway

• hexosw monophosphate shunt

pathway when we need energy production

glycogenesis

done when there are extra glucoses in the body in the form of glycogen

embden-meyerhof pathway

• Form of anaerobic glycolysis

• Conversion of glucose into 2 three-carbon molecules pyruvate/pyruvic acid in the cell cytosol, can further metabolized to lactate

• Requires 2 ATP; creates 4 ATP; net gain of 2 ATP

Glycerol

released from the hydrolysis of triglycerides can enter 3-phosphoglycerate

Fatty acids, ketones, some amino acids

can be converted or catabolized to acetyl-CoA before entering TCA cycle

Other amino acids

can enter the pathway as pyruvate or as α-ketoacids and α-oxoacids

gluconeogenesis

• conversion of of amino acids to substrates that can be

converted to glucose by the liver and kidney

• conversion of glycerol, lactate and pyruvate to glucose

anaerobic glycolysis

• Important for muscle, which often has important energy requirements without an adequate oxygen supply → can derive ATP from glucose in an oxygen-deficient environment by converting pyruvic into lactic acid

• Requires 2 ATP for 1 glucose; creates 4 ATP; net gain of

  2 ATP

• lactic acid

• systemic circulation

anaerobic glycolysis

• — → diffuses from muscle cells → enters the

  — → taken up and used by the liver

electron transport chain

anaerobic glycolysis

• Gains ATP from introduction of pyruvate into TCA and NADH into —

hexose monophosphate

• detour of glucose-6-phosphate to 6-phosphogluconic

acid

• 6-PGA permits the formation of ribulose-5-phosphate (or

pentoses) and NADP to NADPH (reduced form)

nadph

• important to mature erythrocytes (no mitochondria; incapable of TCA cycle)

• reducing power protects cell lipid bilayer membrane and

critical enzymes from oxidative and free radical damage

resulting to cell death

glycogenesis

excess glucose can be stored as glycogen (by liver and muscle)

• glucose-1-phosphate

• glycogen synthase

conversion in glycogenesis

• glucose-6-phosphate→ — →uridine

  diphosphoglucose→glycogen by —

hepatocytes

are capable of the synthesis of glycogen, or other sources to maintain the blood glucose concentration → because liver is able to

synthesize enzyme glucose-6-phosphatase

glucose-6-phosphatase

without —, glucose is trapped in glycolytic pathway

muscles

incapable of dephosphorylating glucose → because it do not synthesize

glucose-6-phosphatase

catabolized

glucose enters muscle cell → remains as glycogen unless —

glycogenolysis

Process which glycogen is converted back to glucose-6-phosphate for entry into the glycolytic pathway

glycolysis

metabolism of glucose molecule to pyruvate or lactate for production of energy

gluconeogenesis

formation of glucose-6-phosphate from noncarbohydrate sources

glycogenesis

breakdown of glycogen to glucose for use as energy

glycogenesis

conversion of glucose to glycogen

lipogenesis

conversion of carbohydrates to fatty acids

lipolyis

decomposition of fat

glycogenesis

process in the pathway for hyperglycemia

glycogenolysis

process in the oathway for hypoglycemia

insulin and glucagon

Two main hormones that control blood glucose: — produced by the pancreas

insulin

• Is synthesized by the β-cells of islets of Langerhans in the pancreas

• Normally released when glucose levels are high

• Is responsible for the entry of glucose into the cell

hypoglycemic agent

only hormone that decreases blood sugar level

glucagon

• Is synthesized by the α-cells of islets of Langerhans in the pancreas

• Is released during stress and fasting states

hyperglycemic agent

primary hormone that increases blood glucose level

epinephrine

• adrenal medulla

• inhibits insulin secretion

• increases glycogenolysis and lipolysis

glucocorticoids

• adrenal cortex

• decreases intestinal entry into the cell

• increases gluconeogenesis and lipolysis

growth hormone

• pituitary gland

• decreases the entry of glucose into the cells and increases glycogenolysis

• its release from the pituitary is stimulated by decreased

• glucose levels and inhibited by increased glucose

adrenocorticotropic hormone

• pituitary gland

• its release is stimulated by decreased levels of cortisol

Hypothalamic-Pituitary-Adrenal Gland Axis

for diabetic patients, hormones like these are stress hormones.

thyroxine

• thyroid gland

• by increasing glycogenolysis, gluconeogenesis, and

intestinal absorption of glucose

somatostatin

by the inhibition of insulin, glucagon, growth hormone,

and other endocrine hormones

- Soloflight hormone

diabetes mellitus

A group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both

National Diabetes Data Group, 1979

■ Type 1, insulin-dependent diabetes mellitus (IDDM)

■ Type 2, non-insulin-dependent diabetes mellitus (NIDDM)

International Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1995

■ Type 1 and Type 2

• Type 1 diabetes

• Type 2 diabetes

• Other specific types of diabetes

• Gestational diabetes mellitus (GDM)

new categories of diabetes by ada and who

type 1 diabetes

• Insulin-dependent DM, Juvenile Onset DM, Brittle Diabetes, Ketosis-Prone diabetes

• Result of cellular-mediated autoimmune destruction of

  the β-cells of the pancreas, causing an absolute

  deficiency of insulin secretion

• coxsackievirus b

• rotavirus

• mumps virus

viruses that are associated with type 1 diabetes

Juvenile Onset DM

Usually diagnosed in children, teens and young adults

brittle diabetes

Absolute insulin deficiency occurs because β-cells cannot produce insulin

due to autoimmune destruction

ketosis-prone diabetes

production of ketone bodies coming from fat bodies

Latent Autoimmune Diabetes of Adulthood

A slower autoimmune β-cell destruction that can occur in adults

idiopathic type 1 diabetes

has no known etiology; strongly inherited; does not have

β-cell autoimmunity; requires insulin replacement

type 2 diabetes

● Non-insulin Dependent DM, Maturity Onset or Adult Type DM, Stable Diabetes, Ketosis-resistant Diabetes, Receptor-Deficient DM

● A result of an individual’s resistance to insulin with an insulin secretory defect (relative insulin deficiency)

ketoacidosis

Decreased production of ketone bodies

Polyendocrine metabolic ovarian syndrome

new name of PCOS

metformin

lower blood sugar + regularized menstrual cycle

macrovascular and microvascular

complications in type 2 diabetes

brain tumor (meningioma)

- increased brain pressure

- Administer dexamethasone (steroid) to increase blood sugar levels

Cushing’s syndrome

excessive cortisol production

Pheochromocytoma

catecholamine-secreting tumor

acromegaly

excessive production of growth hormone

hyperthyroidism

high thyroid hormones

dilantin and pentamidine

inducers of B-cell dysfunction

thiazides

impair insulin action

down syndrome

linked to type 1 autoimmune diabetes

gestational diabetes

Any degree of glucose intolerance with onset or first recognition during second or third trimester of pregnancy

respiratory distress syndrome

They experience difficulty breathing and collapsed alveoli

surfactant

is responsible for keeping the air sacs or alveoli open. If surfactant synthesis is inhibited, the alveoli may collapse.

hypocalcemia

decrease in blood calcium levels

fetal hyperinsulinemia

Maternal hyperglycemia can lead to

hyperbilirubinia

liver can’t properly process bilirubin