Body Weight And Obesity/diabetes SEM2 Flashcards

1
Q

What is the “set-point” of body weight

A

Predetermined set point which the body seeks to maintain homeostasis

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2
Q

What are the key brain regions involved in appetite control

A

Hypothalamus
Brainstem
Reward and sensory processing areas

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3
Q

What is the hypothalamuses involvement in appetite regulation

A

Central to appetite regulation
Contains arcuate nucleus

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4
Q

What are the two important neurone types in the arcuate nucleus

A

Anorexigenic - satiety
Orexgingenic - hunger

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5
Q

What can removing orexigenic arcuate neurones result in

A

Can result in starvation

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6
Q

What does the use of optogenietic approaches allow for

A

Control of specific population of neurones, activation of orexigenic arcuate AgRP neurones increase in food intake

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7
Q

What leads to a reduction in food intake and body weight

A

Stimulating the anorexigenic POMC in the arcuate nucleus

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8
Q

What are NPY/AgRP neurones

A

Orexigenic

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9
Q

What are POMC neurones

A

Anorexigenic

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10
Q

What occurs if the gene of leptin is removed

A

The leptin hormone is no longer able to send signals to the brain to inhibit hunger

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11
Q

What are the results of leptin acting on arcuate POMC cells

A

Leptin increases POMC mRNA expression
Leptin excites POMC cells electrophysiologically

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12
Q

What happens to leptin activity in relation to obesity

A

Leptin target sites can become insensitive to leptin in obesity

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13
Q

What can partial leptin reduction restore

A

Restores hypothalamic leptin sensitivity and leads to reduced food intake

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14
Q

What does the binding of leptin lead to

A

Leads to dimerisation (pairing) of the receptor - essential for activation of the signalling pathway

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15
Q

What does the activation of the leptin receptor trigger

A

Triggers the activation of JAK2 which phosphorylates itself and other proteins (+ leptin receptor)

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16
Q

What is a important pathway activated by JAK2

A

The STAT3 (signal transducer and activator of transcription 3) pathway

17
Q

What does SOCS3 act as in the leptin signalling pathway

A

Acts as a negative feedback regulator by inhibiting JAK2 activity - can lower the leptin signalling pathway

18
Q

What may happen to SOCS3 levels with chronically high levels of leptin (seen in obesity)

A

SOCS3 levels elevated contributing to leptin resistance by inhibiting leptin signalling pathways

19
Q

What is hyperglycaemia and how its caused

A

Hyperglycaemia is excessive circulating glucose
Mainly caused by fluid loss via an osmotic effect

20
Q

What is hypoglycaemia and how is it caused

A

Hypoglycaemia is insufficient circulating glucose
Mainly caused by lack of glucose

21
Q

How is insulin synthesised

A

Synthesised in β cells in the pancreas

22
Q

What is insulin released in response to

A

Released in response to an increase in blood glucose

23
Q

Where is glucagon synthesised

A

Synthesised in α cells in the pancreas

24
Q

What is glycogen

A

A polymer of glucose stored and released by the liver

25
Q

What is gluconeogenesis

A

The process of generating new glucose molecules from non-carbohydrate sources by the liver

26
Q

How does glucagon act

A

Acts to oppose insulin actions by stimulating hepatic glucose synthesis and mobilisation

27
Q

What does the pancreas release

A

Insulin and glucagon

28
Q

What is type 1 diabetes a result of

A

Result of deficiency in insulin production due to autoimmune destruction of β cells in the pancreas
Onset in childhood

29
Q

What is type 2 diabetes a result of

A

Result of a lack of sensitivity to insulin
Insufficient insulin production from β cells after period of insulin resistance