Obesity and diabetes Flashcards
deck complete
energy stores in the body
plasma glucose
glycogen (liver)
glycogen (muscle)
triacylglycerol (adipose, muscle)
protein
fuels in the blood
glucose
fatty acids
ketone bodies
aminoacids
lactate
what is formed by glycerol and phosphoenolpyruvate
glucose
what is formed by glucose in gluconeogenesis
phosphoenolpyruvate
what is formed by phosphoenolpyruvate
pyruvate
what is formed by lactate
pyruvate
what is formed by pyruvate
oxaloacetate
acetyl-CoA
what forms acetyl-CoA
ketogenic aminoacids
fatty acids
ethanol
pyruvate
what is formed by acetyl-CoA
acetoacetate
what does acetoacetate form and what is acetoacetate formed by
3-hydroxybutyrate
what glucogenic aminoacids are involved in gluconeogenesis and ketogenesis in the liver
oxaloacetate
fumarate
2-oxoglutarate
starting with the acetyl-CoA entry point, what is the cycle of ketogenesis in the liver
citrate
isocitrate > CO2
2-oxoglutarate > CO2
fumarate
malate
oxaloacetate
what is gluconeogenesis
the process of making glucose from its own breakdown products or from the breakdown products of lipids or proteins
what is ketogenesis and when does it take place
- a metabolic pathway that produces ketone bodies which provide an alternate form of energy for the body
- takes place when the body lacks sufficient carbohydrates to burn for energy
what is insulin
‘the hormone of the fed state’
functions of insulin in the liver
increased glycogen synthesis
decreased glycogenolysis
decreased gluconeogenesis
functions of insulin in the muscle
increased glucose uptake
increased glycogen synthesis
decreased glycogenolysis
increased protein synthesis
functions of insulin in adipose tissue
increased glucose uptake
increased TAG synthesis
decreased lipolysis
type 1 diabetes mellitus
insulin dependent
failure of insulin production
10-20% of cases
clinical signs of type 1 diabetes mellitus
early and rapid onset
weight loss
hyperglycaemia
ketonaemia
symptoms of type 1 diabetes mellitus
polydipsia
polyuria
metabolic acidaemia
type 2 diabetes mellitus
non-insulin dependent
loss of insulin sensitivity
80-90% of cases
clinical signs of type 2 diabetes mellitus
slow onset (usually aged >35 years)
frequently associated with obesity
hyperglycaemia
symptoms of type 2 diabetes mellitus
retinopathy
nephropathy
neuropathy
heart disease
circulatory problems
effects of type 1 diabetes
insufficient/ineffective insulin produced
liver - hyperglycaemia
muscle - hyperglycaemia, weight loss
adipose - ketoacidaemia, weight loss - due to decreased TAG synthesis and increased lipolysis
effects of type 2 diabetes
insulin produced but not detected
liver, muscle and adipose - hyperglycaemia
adipose - due to increase TAG synthesis and decreased lipolysis
metformin
drug used in treatment of type 2 diabetes
inhibits gluconeogenesis
activates AMP-activated protein kinase
acts on intestine
metabolic effects of AMP-activated protein kinase
increased:
- glucose uptake
- glycolysis
- fatty acid oxidation
- mitochondrial biogenesis
decreased:
- rRNA synthesis
- protein synthesis
- triacylglycerol synthesis
- fatty acid synthesis
- cholesterol synthesis
- glycogen synthesis
- gluconeogenesis
metabolic syndrome
affects 20-30% population, males > females
increased abdominal fat
dyslipidaemia
insulin resistance
impaired glucose tolerance
high blood pressure
cardiovascular disease
energy intake
food intake
energy expenditure
basal metabolism 60%
physical activity 30%
digestion 10%
thermogenesis
role of microbiome in obesity
co-evolution with host
fermentation of complex carbs > short chain fatty acids
metabolic health correlated with diversity of gut bacteria
leptin
peptide hormone
released by adipocytes
circulating levels correlate with body’s fat content
leptin receptors in brain including hypothalamus
suppression of food intake = motivation to eat, rewards for feeing, satiety
increased metabolic rate
hormones affecting digestion
ghrelin
cholycystekinin
gastric inhibitory peptide
peptide YY
ghrelin
screted by gastric cells
orixigenic - increases hunger
levels fall after feeding
inhibits insulin secretion
cholecystekinin
secreted by duodenum
stimulates secretion of digestive enzymes and bile
slows gastric emptying
anorexigenic - causes loss of appetite
gastric inhibitory peptide
secreted by duodenum, jejunum
inhibits gastric acidification, slows digestion
stimulates insulin secretion
peptide YY
secreted by ileum, colon
anorexigenic
