Metabolic homesotasis

  • Created by: LUFCMazza
  • Created on: 10-08-20 18:13
Insulin like grwoth factor 1 )IGF1)
major hormonal determinant of foetal growth. Expressed in all tissues and the placenta. Paracrine and endocrine effects are in play, as well as bioavailability and the levels of IGF binding proteins present
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Insulin like grwoth fator 2
late foetal blood mainly has IGF2 bu 1 has greater biologicla effects.
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When does it appear
after organogenesis but acts through IGF1. Effects not mediated thorugh insulin
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Placenta is a source of
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PLacental glucose transfer- foetal insulin release- IGF1 release.
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Foeal pancreas
leads to low levels of IGF1 and intra-uterine grwoth retardation. Maternal starvation may lead to low IGF1 and this can be relieved by infusion of either insulin or glucose. Insulin also promotes deposition of adipose tissue
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Growth hormones...
levles are high in foetus, but few receptors are foudn in peripheral tissue. GH from the placenta is transported to the maternal circulation and suppresses maternal pituitary GH release, may help in regulation of IGF1 levels
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Hormonal abnormalities.. diabetic mothers:
maternal hyperglycaemia leads to foetal hyperinsulinaemia = increases foetal insulin secretion = fat
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Pancreatic agenesis...
leads to a reduction in body weight
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failure of insuli receptor = severe dwarfism
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what is Beckwith-Wiedemann syndrome
excessive iGF2 production and somatic overgrwoth. IgF2 gene closely linked with H10 gene for a non-coding RNA that regulates IGF2 expression. IGF2 is on paternal allele and H19 on maternal allele
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Paternal chromosome...
H19 promoter is methylated so enhancer doesn't bind. Enhancer binds IGFlittle H promoter isntead and activates expression
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Maternal chromosome
H19 is unmethylated so the enhancer acts locally to activate expression of this and ther eis no enhancer activity to activate the IGF2 gene
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What What's obese BMI
BMI of 30-40 is obese. BMI of more than 40 is severely obese
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Ghrelin is secreted by
stomach and stimulates apetite by activationo f NPY and AgRP in the arcuate nucleus of hypothalamus via GHS-R1a receptors
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NPY adn AgRP?
are orexigenic
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What does it inhibit?
POMC which as anorexigenic
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Also stimulates
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Peripheral effects of ghrelin?
decreased glucose stimulated insulin secretion, decreased fatty acid use as fuel, increae sapeptide via AMPK and on liver AMPK- more gluconeogenesis and fat syntehsis too also acts on adipose tossue for more fat accumulation
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increaes glucose uptake. Upregulates lipoprotein lipase activity (for breakdown of chylomicrons/VLDL into fatty acids for uptake)
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acylaton stimulating protein (to ocnvert FA into TG for storage)
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HSL actiivty (converts TG into FA for release from the cell)
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IN obestiy?
suppresison of FA relase by insulin is reduced so more FA is relased. Activation of liporpotein lipase is reduced, so less clearance of chylomicron/ VLDL
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insuffieicnet fat tisseu to buffer plasma lipids = systemic lipid delivery = TG accumulation in muscle, liver and pancreas - lipotoxicity thus insulin resistance adn eventually faliure in insulin secretion
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adipose tissue...
leptin is produced by adopose cells, regulates food intake,
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where does leptin act>
leptin acts on hypothalamus to activate POMC and inhibit NPY. Peripehrelaly influences insuin secretion
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weight loss
reduces leptin, relieves inhibition of NPY = increased food intake.
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insulin promotes...
leptin secreiton by adipocytes.
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acts to decrease lipogenesis and increase lipolysis, limits excessive TG storage. Blocks insulin signalling via interfernece with intracellular signal transduction and decreased expression of GLUT4 transporters. Produced in obese humans by adipose
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MOS infiltrates
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related to TNFa and collagen- reduces hepatic glucose production and increases muscle glucose utlisation. levels reduced in obesity so too much glucose production in liver and lowered muscle glucose ultisation
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what increaes levels
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Acylation stimulating protein
o Derived from complement factor 3, acts on adipocytes to increase TG formation by increasing glucose uptake and TG synthesis (additive effect with insulin) o Suppression of lipolysis and fatty acid release o Levels are increased in obese people and
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and fall after weight loss o Regulatory effects may be lost due to metabolic disturbances since increased levels don't counteract the metabolic abnormalities • Interleukin 6 • Plasminogen activator inhibitor I`
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insulin resistance
really obvious. Leptin normlaly sensitises tissue to insulin. adiponectin promotes uptakeand oxidationo f atty acids
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Folic acid
prevention of neural tube defects
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Vitamin D
for healthy bones and teeth...insufficiency leads to bone deformities such as rickets in children and osteomalacia in adults
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Diabetes mellitus
pancreas has acinar cells grouped into lobules to secrete enzymes into common duct and release secretions into duodenum
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when are islets of Langerhns
distinguishable from 12th week embryo
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complex blood supply
superior and inferior pancreaticoduodenal arteries
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drains into portal vessels
passing to liver
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innervation of pancreas is via the
coealia plexus (ANS), sympathetic innervation form coeliac plexu (ANS), sympathetic innervation from coeliac ganglin and parasympathetic innervation from vagus nerve
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alpha cells
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beta cells
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delta cells
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gamma cells
pancreatic polypeptide
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islets of Langerhans...
disperse endocrine glands scattered throughout the exocrine pancreas
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exocrine means
protease are released into ducts which drain into central duct connecting to teh SI
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cells release products directly into circulaiton for transprot to target tissues
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diabetes mellitus... type 1
complete lack of insulin, beta cells are destroyed (autoimmune destruction)
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type 2
severe resistance to insulin but some insulin remains. imparied B cell function and defective insulin signlaling boserved in metabolic syndrome and obese patients
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neonatal diabtes
mutaiotns in Katp
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More insulin released when glucose is high- Katp close so K+ high in cell. CLOSED KATP MEANS MROE INSULIN IS RELASED.
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Neonatal diabetes
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What can close Katp?
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What is congenital hyperinsulinaemia?
Means Katp channels are clsoed and so insulin secretion is upregulated
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on membranes of all cells- basal uptake of glucose
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small intestine, renal tubules, hepatocytes, brain and beta cells
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skeletal, cardiac and adipose
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gut= fructose
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SGLT1 and 2
co-transporters of glucose against conc gradient
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GLUT 5 and 2
work togehter- 5 absorbs fructose and 2 shoves it into circulation
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activates GLUT esp VLUT 4--- GLUT 4 translcoated into cell membrane
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oral hypoglycaemic, is a sulphonylureas which binds to SUR1 receptors on pancreatic B cells to close the Katp channels and decrease efflux of K ions - cell is depolarises and this causes voltage dependent Ca2+ channels to open to give ca2+ influx ->
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Ca2+ binds to activate calmodulin and this leads to exocytosis of insulin vesicles -> insulin released
..for type II diabetes, suppress glucose production by the liver (gluconeogenesis) since the diabetics have more than normal levels of gluconeogenesis. Thought to be through activation of AMPK (AMP activated protein kinase)
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(peroxisome proliferator-activated receptors) are TFs expressed in adipose tissue to regulate adipocyte differentiation and direct activator of genes for enzymes of lipid metabolism.
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o Thiazolidenediones are ligand agonists for PPARy - stimulate adipocyte differentiation and lower glucose and FFA concentrations and increase whole body insulin sensitivity o TZDs improve insulin sensitivity in type II diabetes
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Insulin like grwoth fator 2


late foetal blood mainly has IGF2 bu 1 has greater biologicla effects.

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When does it appear


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Placenta is a source of


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