Absorptive State Flashcards
- What is the fate of glucose in the liver, muscle, adipose tissue, and other tissues?
- What is the fate of amino acids in the liver and muscle?
- What is the fate of triglycerides in adipose tissue?
1. liver = glycogen, TG in XS muscle = glycogen adipose = TG other = Krebs cycle for energy 2. liver = ketoacids for energy muscle = protein 3. hydrolysed into free fatty acids and glycerol, reesterified back into fat
Control of absorptive state:
- Switch from post absorptive to absorptive state due to increased ………. and ……….. in blood
- Insulin - secreted by …….. ……. . Trigger is …………..and ………. ………..
- ……….. is the transporter responsible for Bcell glucose uptake. This triggered the generation of …… from glucose metabolism and …… influx.
- The raised intracellular …… causes insulin exocytosis
- glucose and insulin
- bcells, glucose and AA’s
- GLUT2, ATP, Ca2+
- Ca2+
By what transporter is glucose taken up in cells?
GLUT-4
What are the effects of insulin on: - liver - adipose - muscle What are the transporters involved?
Liver = GLUT-2 (insulin insensitive), inhibits glycogenolysis, stimulates glycogen synthesis, drives lipogenesis if XS glucose Muscle = GLUT-4 (insulin sensitive), recruitment of GLUT-4, stimulates glycogen synthesis, promoting protein synthesis Adipocytes = recruitment of GLUT-4, promote lipogenesis, inhibits lipolysis, increases the synthesis of lipoprotein lipase (acts on chylomicron to release fatty acids)
What 2 parts make up the post-absoptive state? Which is the most important?
- glucose-supplying reactions - generate glucose
2. glucose sparing reactions - generate other substrates such as FA’s and ketone bodies MORE IMPORTANT
What are the 2 glucose supplying reactions?
glycogenolysis
gluconeogenesis
What 3 things can go to the liver to produce glucose? Where do they come from?
amino acids - muscle
lactate - muscle
glycerol - adipose
What is the main regulator of glucose-supplying reactions?
What 4 hormones can affect it?
fall in insulin levels
epinephrine, increases glycogen breakdown
glucagon, increase glycogen breakdown
cortisol, increases gluconeogenesis, decreases glucose uptake
growth hormone, decreases glucose uptake
What happens in a type 1 diabetic in:
- liver
- adipocytes
- muscles
liver = decreased glycogen synthesis, increased glycogenolysis, ketone bodies formed adipocytes = decreased glucose uptake, increased lipolysis muscles = increased extracellular glucose, breakdown of protein to amino acids as substrate for gluconeogenesis
Summary of metabolic derangement:
- level of glucose in blood is high because …… is not stimulated
- further compounded by lack of insulin mediated inhibition of ……… and ………….
uptake
glycogenolysis
lipolysis
Describe the consequences of increased lipolysis in diabetics, in a series of events.
lipolysis –> FFA go to liver –> beta oxidation –> XS acetyl CoA –> Krebs inhibited –> ketogenesis –> acidosis
Clinical features of uncontrolled diabetes?
polyuria/polydipsia dehydration blurred vision infections e.g. thrush weight loss ketosis confusion coma
What can happen to diabetics when treated rapidly with insulin?
hypokaleamia
What are the 2 categories of long-term metabolic consequences of diabetes?
microvascular
- retinopathy, nephropathy, neuropathy
macrovascular
- atherosclerosis, strokes, heart attacks, peripheral vascular disease