PHTY208 Lecture Notes - Lecture 21: Impaired Glucose Tolerance, Paresthesia, Plantar Reflex
Diabetes Mellitus and the Metabolic Syndrome
• A group of metabolic diseases in which a person has high blood glucose
• Approximately 7% of the population currently have type 2 diabetes but more common in
Indigenous Australians (~20%)
• The most common types of diabetes are:
o Type 1 diabetes: results from the body's failure to produce insulin
o Type 2 diabetes: results from insulin resistance, a condition in which cells fail to use
insulin properly
• Hormonal control of glucose, fat, and protein metabolism
o Glucose, fats and protein
• The body uses glucose, fats and proteins as major energy sources for the body
• The liver, with hormones from the pancreas, regulates energy production
• Glucose is metabolised to CO2 and H2O.
▪ 16 kJ/g
• Fat is metabolised to glycerol and fatty acids
▪ 37 kJ/g
• Protein is metabolised to amino acids
▪ 16 kJ/g
o Tissue types and functions of the pancreas
• Acini
▪ Secrete digestive juices into the duodenum
• Islets of Langerhans
▪ Secrete hormones into the blood
▪ Beta cells that secrete insulin and amylin
▪ Alpha cells that secrete glucagon
▪ Delta cells that secrete somatostatin
o Actions of insulin
• Central to regulating carbohydrate and fat metabolism in the body
▪ Promotes conversion of triglycerides to fat and subsequent storage in
adipose tissue
▪ Promotes glucose uptake by insulin sensitive target cells in muscle and
liver
▪ Provides for glucose storage as glycogen
• Increases glycogen synthesis
▪ Inhibits hepatic gluconeogenesis
▪ Increases protein synthesis
o Actions of glucagon
• Opposite of insulin
▪ Catabolic in nature
▪ Increases transport of amino acids into hepatic cells
• Promotes glycogen breakdown
▪ Increases breakdown of proteins into amino acids for use in
gluconeogenesis
▪ Increases conversion of amino acids into glucose precursors
o Regulation of blood glucose
find more resources at oneclass.com
find more resources at oneclass.com
o Other hormones affecting blood glucose
• Catecholamines
▪ Epinephrine and norepinephrine
▪ Help to maintain blood glucose levels during periods of stress
• Growth hormone
▪ Increases protein synthesis in all cells of the body, mobilises fatty acids
from adipose tissue, and antagonises the effects of insulin
• Glucocorticoids
▪ Critical to survival during periods of fasting and starvation
▪ Stimulate gluconeogenesis by the liver
• Diabetes
o Diabetes Mellitus
• Disorder of carbohydrate, protein, and fat metabolism
▪ Results from an imbalance between insulin availability and insulin need
• Can represent:
▪ An absolute insulin deficiency
▪ Impaired release of insulin by the pancreatic beta cells
▪ Inadequate or defective insulin receptors
▪ Production of inactive insulin or insulin that is destroyed before it can
carry out its action
• Has a common feature of hyperglycaemia
• Types
▪ Prediabetes:
• Impaired fasting plasma glucose, FPG – 5.6 – 6.9 mmol/L
• Impaired glucose tolerance, OGTT – 7.8 – 11.0 mmol/L
• Increased risk of atherosclerotic heart disease and increased risk
of progression to type 2 diabetes
• Diabetes: >11.1 mmol/L or > 7 mmol/L fasting
▪ Type 1 results from:
• Loss of beta cell function
• An absolute insulin deficiency
• Type 1A - Immune-mediated diabetes
• Type 1B - Idiopathic diabetes
▪ Type 2 results from:
• Impaired ability of the tissues to use insulin
• A relative lack of insulin or impaired release of insulin in relation
to blood glucose levels
find more resources at oneclass.com
find more resources at oneclass.com
o Type 1
• Characterised by extensive damage to the pancreatic beta islet cells
• Two main forms
▪ Type 1a
▪ Type 1b
• Insulin production and release is reduced
• Can be insidious or rapid onset
• Body can compensate and the condition can go undiagnosed for years
• Development of type 1A
▪ Genetic predisposition
▪ Immunologically mediated beta cell destruction
• Insulin antibodies or islet antibodies
▪ Formerly juvenile diabetes
▪ More common in young persons but can occur at any age
▪ A hypothetical triggering event involving an environmental agent that
incites an immune response
• Infection, hypersensitivity reaction, prolonged major stressful
event
▪ Prone to the development of ketoacidosis
• Insulin inhibits lipolysis and releases free fatty acids
• Without insulin ketosis develops and are converted to ketones in
the liver
• Idiopathic Type 1B Diabetes
▪ Those cases of beta cell destruction in which no evidence of
autoimmunity is present
▪ Only a small number of people with type 1 diabetes fall into this
category
▪ Strongly inherited.
▪ People with the disorder have episodic ketoacidosis due to varying
degrees of insulin deficiency with periods of absolute insulin deficiency
that may come and go.
o Type 2
• Heterogeneous condition that describes the presence of hyperglycaemia in
association with relative insulin deficiency
▪ Peripheral insulin resistance
▪ Impaired beta cell function and insulin secretion
▪ Increased hepatic glucose production
• Associated with overweight and obese persons
• Environmental and genetic origins
▪ Could be 20 or more genes responsible
• Causes of Beta Cell Dysfunction
▪ An initial decrease in the beta cell mass
▪ Increased beta cell apoptosis/decreased regeneration
▪ Long-standing insulin resistance, leading to beta cell exhaustion
▪ Chronic hyperglycaemia can induce beta cell desensitisation
glucotoicit.
▪ Chronic elevation of free fatty acids can cause toxicity to beta cells
lipotoicit.
▪ Amyloid deposition in the beta cell can cause dysfunction.
• Type 2 diabetes
▪ Individuals can have low to normal to high levels of insulin
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Diabetes mellitus and the metabolic syndrome: a group of metabolic diseases in which a person has high blood glucose, approximately 7% of the population currently have type 2 diabetes but more common in. Fat is metabolised to glycerol and fatty acids: 37 kj/g, protein is metabolised to amino acids, 16 kj/g, tissue types and functions of the pancreas, acini. Increases protein synthesis: actions of glucagon, opposite of insulin, catabolic in nature. Increases transport of amino acids into hepatic cells: promotes glycogen breakdown. Increases breakdown of proteins into amino acids for use in gluconeogenesis. Increases conversion of amino acids into glucose precursors: regulation of blood glucose, other hormones affecting blood glucose, catecholamines, epinephrine and norepinephrine, help to maintain blood glucose levels during periods of stress, growth hormone. Increases protein synthesis in all cells of the body, mobilises fatty acids from adipose tissue, and antagonises the effects of insulin: glucocorticoids, critical to survival during periods of fasting and starvation.
