Lecture 10 - Dysregulation of Glucose and Fat Metabolism Flashcards
(38 cards)
what is the genetic predisposition of type 1 diabetes compared with type 2
type 1 = moderate
type 2 = very strong
what is the frequency of ketosis in type 1 and type 2 diabetes
type 1 = common
type 2 = rare
what is the problem in type 1 diabetes
B cells are destroyed, eliminating production of insulin
what is the problem in type 2 diabetes
insulin resistance combined with inability of B cells to produce appropriate quantities of insulin
what is the fasting + random glucose level that is a symptom of diabetes
fasting glucose > 7mmol/L or random >11.1 mmol/L
what level of HbA1c be a symptom of diabetes and why
HbA1c > 50 mmol/mol
- higher levels than this would suggest that you have had elevated glucose levels for sometime
what are some symptoms of diabetes
- thirst
- frequent urination
- fatigue
- hyperventilation
- blurred vision
- coma
what are glycosuria, osmotic diuresis and dehydration common symptoms of
diabetes
what are the three stages that lead to the development of diabetes from obesity
- obesity
- insulin resistance
- glucose intolerance
- metabolic syndrome
- type 2 diabetes
what can not be distinguished between a normal and obese pre diabetic
can not distinguish between the obese and normal patient from glucose levels in the blood
what do insulin resistant obese people require more of
require more insulin to get the same glucose control as a normal person
= this is what you can the difference btwn normal and obese on graph
over time what happens to a insulin resistant diabetic over time in the control of blood glucose
over time, lose the control of blood glucose as their levels are constantly high and never properly go back down before the next meal
what does insulin resistance mean
reduced response to the same amount of insulin
what does hyperinsulinaemia diminish
the ability of b cells to respond to further increase in blood glucose
during insulin resistance, what happens to the processes that are normally stimulated by insulin
they arent stimulated
during insulin resistance, what happens to the processes that are normally inhibited by insulin
they aren’t inhibited
what are things that are normally stimulated which aren’t during insulin resistance (what happens to them)
- glucose uptake
- glycolysis
- fatty acid uptake
are decreased
what are things that are normally inhibited which aren’t during insulin resistance (what happens to them)
- gluconeogenesis
- lipolysis
- fatty acid oxidation
- ketogenesis
are increased
what happens to gluconeogenesis and fat mobilisation in type 2 diabetes
processes are increased as they are no longer inhibited by insulin
what happens to the phosphorylation of proteins in the signalling pathway during insulin resistance
some proteins that would usually be phosphorylated are either not or incorrectly phosphorylated
what are the two theories about how insulin resistance develops and what is there evidence that they both do
- oxidative stress
- inflammation
evidence that they both alter the insulin signalling pathway
how does oxidative stress lead to insulin resistance
overweight people often have a high flux of glucose and lipid into the mitochondria
high activity of the electron transport chain can cause oxidative stress
this can cause miss phosphorylation of parts of the insulin signalling pathway
how does inflammation lead to insulin resistance
pro-inflammatory cytokines can activate serine/threonine kinases, which can interrupt the normal pathway of insulin signalling
are all tissues and pathways affected equally by insulin resistance
no
