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Nutrients & Metabolic Disease > LT3 Body Nutrient Status > Flashcards

LT3 Body Nutrient Status Flashcards

1
Q

What causes obesity?

A

Imbalance of foot intake and energy expenditure

Suggestesd that defective neuronal network regulation via ANS = in turn induces flobal changes in nutrient and energy flux

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2
Q

What information is sent to the brain in obesity?

A

Energy stores
Food intake - amount and type
Immune status - microbiome

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3
Q

What in the periphery has to be controlled?

A

Substrate utilizaiton and storage

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4
Q

Describe the flow of information

A

Bi-directional

2nd order neurones can also signal back to 1st order

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5
Q

What type of inputs from from periphery to CNS?

A

Both neuronal and endocrine

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6
Q

Where do satiety signals come from and what do they control?

A

‘meal size’

Information from upper GIT via vagus and sympathetic afferents converge on NTS and hypothalamus

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7
Q

What does NTS stand for?

A

Nucleus of the solitary tract

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8
Q

What are the long term and short term signals about energy stores?

A

Satiety signalling = short term

Adiposity negative feedback signalling = long term

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9
Q

Define satiation

A

Senesation of fulln ess generated during a meal

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10
Q

Define satiety

A

Period of time between end of one meal and start of the next

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11
Q

Define adiposity

A

State of being obese

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12
Q

What does short-term satiety signalling regulate?

A

Meal initiation, termination adn inter-meal frequency

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13
Q

What signals are generated by the GIT?

A

Satiation signals
CCK
PYY
GLP-1
OXM
Obestatin

All increase signalling durign meal to supress food intake and appetite

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14
Q

What happens to satiation signals during meal?

A

Satiation signal increases during meal to limit meal size

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15
Q

What is the role of CCK?

A

CCK cells are concentrated in the proximal small intestine.
CCK hormone
is secreted into the blood upon the ingestion of food.

The physiological actions
of CCK include stimulation of pancreatic secretion and gallbladder contraction,
inhibits gastric emptying, and induction of satiety.

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16
Q

Where does CCK signal to in the brain?

A

Signals to hindbrain NTS

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17
Q

What is the role of PYY?

A

Inhibits gastic motility & reduces food intake

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18
Q

Where is PYY secreted from?

A

L-cells in the gut

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19
Q

What is the role of GLP-1?

A

Inhibits gastric emtyping and reduces food intake

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20
Q

Where is GLP-1 released from?

A

L-cells of the gut

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21
Q

What two satiety signals are released from L-cells in the gut?

A

PYY and GLP-1

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22
Q

Why are PYY and GLP-1 considered hypo?

A

Because they have a significant effect on lowering blood sugar levels by stimulating insulin secretion and suppressing glucagon release, essentially promoting a hypoglycemic state when their levels are elevated, particularly after a meal when they are naturally released in the gut.

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23
Q

What is the role of oxyntomodulin (OXM)?

A

Suppresses appetite

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24
Q

What is the role of obestatin?

A

Anorexigenic = suppresses food intake

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25
Q

What does NTS do?***

A

Key integrative centre?

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26
Q

What neural route does long-term satiety signalling go through?

A

Adipose and pancreas signal thorugh ARC

Signal eventually delivered to NTS

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27
Q

What neural route does short-term satiety signalling go through?

A

Stomach and GIT signals both to ARC and to NTS (both via SNS afferent and vagus)

Liver signals via vagus nerve to NTS

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28
Q

Where is leptin predominantly made and released?

A

White adpiose cells

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29
Q

Explain the difference between ob/ob and db/db mice?

A

ob/ob mice = leptin deficient

db/db mice = LEPR b isoform deficient

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30
Q

What type of hormone is leptin?

A

Pleiotropic hormone = a hormone that influences multiple traits or phenotypes.

This means that a single hormone can have multiple functions and act at different levels in the body.

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31
Q

What symptoms do ob/ob and db/db mice have?

A

Causes morbid obesity and T2D leading to:

Hyperphagia = a feeling of extreme, insatiable hunger
Decreased energy expenditure
Insulin resistance
Hyperglycaemia
Metabolic dysfunction

32
Q

What happens when leptin is given to ob/ob mice?

A

Rapidly restore glycaemic control (independent of food intake)

CNS leptin reduces gluconeogensis & glycogenolysis
Suppresses lipogenesis in white adipose tissue

33
Q

What systems if leptin required for?

A

Normal functio of immune and reproductive system

Important for regulation of blood pressure

34
Q

What role does leptin play in puberty?

A

Regulates onset of puberty
Think women enter puberty later than heavier counterparts

Extremely thin women stop ovulating

35
Q

What role does leptin play in angiogenesis?

A

Leptin enhances angiogenesis = formation of blood vessels

36
Q

What other hormones may leptin regulate?

A

May act to regulat the synthesis, release and actions of other hormones

Insulin
Glucocorticoids
Growth hormone

37
Q

What effect does leptin have in tumours?

A

Enhances proliferation = poss thorugh enhancing angiogenesis

38
Q

How is bone growth in ob/ob mice?

A

Reduced bone growth

This is corrected by leptin

39
Q

What 5 areas does leptin act on?

A

Brain
Bone and Cartillage
Vascular function
Reproduction
Immune system

40
Q

Why are there isoforms of the LEPR?

A

Because LEPR mRNA has multiple splice variants

41
Q

Where is LEPRb isoform found abundantly?

A

Hypothalamus = ARC, LHA, VMH

42
Q

Which LEPR isoform allows leptin to cross the BBB?

A

Possible a or c

43
Q

What is correlated with plasma leptin levels?

A

Adipose tissue mass

So high leptin = high adipose tissue mass

44
Q

When does plasma leptin decrease?

A

During fasting because leptin signals fullness

Circulating leptin levels fluctuate with nutritional state

45
Q

What does i.c.v stand for?

A

Intracerebroventricular injection

Route of administration for drugs via injection into the cerebral ventricles so that it reaches the cerebrospinal fluid (CSF)

46
Q

How do we know leptin primarily targets the CNS?

A

Injection of a single dose of leptin i.c.v reduces food intake at doses that have no effect given peripherally

47
Q

What levels of endogenous leptin do obese people have and why?

A

Obesity due to high fat diet = high levels of endogenous leptin

Because there is resistance to actions of leptin
(often associated iwth high levels of circulating insulin and peripheral insulin resistance)

48
Q

What precedes obesity in ob/ob and db/db mice?

A

Hyperinsulinaemia = the body has too much insulin in the blood relative to glucose

49
Q

How would low leptin dose affect ob/ob mice?

A

Does not lower body weight
BUT
Reduces blood glucose and insulin levels in ob/ob mice

50
Q

What is lipodystrophy?

A

Individuals have fewer or no fat cells

Store lipid elsewhere (muscle or liver)

Have high levels of lipid in blood

Fat redistribution syndrome = defective nutrient partitioning

51
Q

What does lipodystrophy tell use about leptin metabolic effects?

A

Leptin metabolic effect are independent of body weight reduction

52
Q

How do you get lipodystrophy?

A

Congenital or acquired (autoimmunity)

53
Q

Symptoms of lipodystrophy?

A

Insulin resistnat
Hyperglycaemic

Those with severe fat deficiency = hyperphagic

54
Q

What is lipodystrophy associated with?

A

Diabetes
LIver steatosis

Common in women = failure to ovulate

55
Q

Where are LEPRb localized?

A

Mainly in ARC neurones

When ARC destroyed and i.c.v leptin added = no longer reduced food intake because receptors were destroyed

56
Q

How does fasting affect mRNA of different neuropeptides?

A

Increases NPY/AgRP mRNA = signalling hunger

Decreases POMC/CART mRNA = signalling satiety

57
Q

What effects on the brain does leptin deficiency have?

A

Reudces brain size and hinders CNS development

Leptin given to NEONATES (not adults) reverses these neuroanatomical defects

58
Q

What brain pathway is disrupted in ob/ob mice?

A

Projection pathway between ARC and PVN

59
Q

ob/ob mice have altered numbers of SYNAPTIC contacts to NYP & POMC neurones copmared to wild type, what are they?

A

Increased EPSCs to NYP/AgRP = promotes hunger

Increased IPSCs to POMC/CART = inhibits satiety

60
Q

How does leptin affect synaptic plasticity?

A

Lack of leptin alters number of excitatory and inhibitory synapses to these neruones

Leptin given to ob/ob mice restored number and type of synaptic connections to wild type

61
Q

How does insulin actin the CNS vs the PNS?

A

While insulin primarily functions in the periphery to stimulate glucose uptake in tissues like muscle and liver, in the brain, its primary role is to regulate central nervous system functions like appetite, cognition, and mood, largely independent of directly influencing glucose uptake, due to the unique characteristics of the blood-brain barrier and specific brain insulin receptors; essentially, insulin has a more “neurotransmitter-like” action in the brain compared to its metabolic role in peripheral tissues.

62
Q

What things are similar about insulin to leptin?

A

Insulin also circulates at levels proportional to body adiposity

Insulin receptors are expressed in hypothalamus (ARC)
Deletion of brain insulin receptor results in obesity

Insulin injected i.c.v inhibits foodintake and reduces body weight in rodents

Insulin i.c.v revereses fasted/diabeic-induced increase in NPY/AgRP mRNA and decrease in POMP mRNA in ARC

63
Q

How does insulin access CNS?

A

Insulin receptor-mediated transport system in brain microvessels = allowing insulin rapid access to CNA

64
Q

How does insulin act in peripheral tissues?

A

Insulin is anabolic and glucoregulatory

Causes hypoglycaemia, increases food intake and energy storage

65
Q

Which neurones have high insulin receptor expression?

A

POMP and AgRP ARC neurones

66
Q

What happens when insulin receptors deleted from POMC and AgRP neurones?

A

Mainly impacts on glucose metabolism rather than food intake and body weight

67
Q

What do AgRP neurones regulate?**

A

They regulate insulin suppression of heptaice glucose suppression

68
Q

Where are components of insulin signalling expressed?

A

Also in ACR neurone

69
Q

What occurs when insulin is delivered to hypothalamus?

A

Modulate hypothalamic neuronal activity = diminish obesity state

Improves whole body insulin sensitivity

Promotes lipogenesis and peripheral fat accumulation (white adipose)

Increases adaptive thermogenesis (“brown” adipose)

70
Q

How does brain insulin resistance affect the obese?

A

Brain insulin levels reduced in genetically obese rats

Insulin-resistant humans have lower CSF:plasma insulin ratio vs insulin sensitive subjects

Hypothalamus shows impairment of proximal insulin signalling components

71
Q

How does brain insulin reduce heptaic glucose production?

A

Insulin acts in ARC to help reduce HGP by inhibition of gluconeogensis

72
Q

What happens when brain insulin receptors are knocked out?

A

Decrease in ability of peripheral insulin to suppress hepatic glucose production

This apprears to be mediated through ARC AgRP neurones

73
Q

What is the pathway of brain insulin reducing hepatic glucose production?

A

Insulin binds receptors on ARC AgRP neurones

Brain inhibits vagal efferents to liver

a7-nAChR causes IL-6 expression in Kupffer cell

IL-6 binds its receptor and activates STAT3

STAT3 dimerizes and represses transcription of gluconeogenic enzymes

74
Q

In a fasting state what happens to increase food intake?

A

Decrease in leptin/insulin

Excitatory synapse at NPY/AgRP = promotes hunger signal

Inhibitory synapse at POMC/CART = decrease in a-MSh released
Inhibits MC3/4 receptor

75
Q

In a fed state what happens to decrease food intake?

A

Increase in leptin/insulin

Inhibitory synapse at NPY/AgRP = inhibits hunger signal less NYP and AgRP released

Excitatory synapse at POMC/CART neurone = increase in a-MSH release which binds MC3/4-receptor

a-MSH binding its receptor = suppresses food intake

Nutrients & Metabolic Disease (13 decks)

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