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biochem block 3 > adipocytes and insulin resistance > Flashcards

adipocytes and insulin resistance Flashcards

1
Q

major regulator of adipocyte functioning in fed state

A

STORAGE

  • insulin
  • increased uptake of glucose into adipocytes to be used for glycerol and also increases activity of LPL to liberate free FA so they can enter adipocytes
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2
Q

regulation of adipocytes in fasted state or when metabolic demand is high

A

LIPOLYSIS

  • epinephrine/glucagon
  • stimulate cAMP –> PKA –> phosphorylates hormone sensitive lipase
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3
Q

what is the action of hormone sensitive lipase?

A

involved in removing FA from triglycerides, most affinity for DAG

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4
Q

outline the reactions from TAG to glycerol + FA in adipose cells

A 
TAG = DAG + FA by desnutrin and HSL
DAG = MAG + FA by HSL 
MAG = glycerol + FA by MAG lipase
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5
Q

describe partitioning of free fatty acids in the fed state

A

in the fed state, FFA that are liberated by LPL are trapped in local adipose tissue so that they are not taken up by cells that are not needing additional energy

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6
Q

describe the use of fatty acids in the fasted state

A

in the fasted state, insulin levels are low and thus epinephrine’s activation of HSL is unopposed. this results in the release of FFA that travel to the liver and are used for ketogenesis or gluconeogenesis

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7
Q

why are upper body adipocytes assoc with increased risk of CVD?

A

upper body adipocytes are larger and larger size = more cytokines and more inflammation

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8
Q

describe leptin

A

adipokine secreted by adipose tissues that acts as a regulator of food intake on the arcuate nucleus of the hypothalamus

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9
Q

what inhibits leptin transcription?

A

PPARg

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10
Q

in most cases of polygenic obesity, leptin levels are actually high, why?

A

leptin levels are high because there is a defect in the signaling pathway (JAK/STAT) - thus “leptin resistance” develops and supplementation does not help

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11
Q

central action of leptin (1)

A

reduce triglyceride content in adipose and non-adipose tissues

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12
Q

peripheral actions of leptin (3)

A
  • stimulate lipolysis
  • reduce expression of acetyl-CoA carboxylase
  • inhibit lipogenesis with inhibition of SREBP-1
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13
Q

current view of leptin

A

signal of energy sufficiency

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14
Q

what is the overall action of adipsin?

A

promotes triglyceride storage in adipocytes and reduce accumulation in liver and muscle

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15
Q

which adipokine has “positive effects”?

A

adiponectin= anti-diabetic, anti-inflammatory, anti-atherogenic

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16
Q

what is the effect of adiponectin in skeletal mm?

A

increases FA oxidation

17
Q

what is the effect of adiponectin in liver?

A
  • decreases FA influx
  • decreased gluose output
  • increases FA oxidation
18
Q

what are the correlations between plasma levels and adiponectin?

A

inverse correlation with triglyceride levels

direct correlation with HDL levels

19
Q

effects of TNFa on adipocytes (3)

A
  • destabilizes lipid droplets to make triglycerides accessible to HSL
  • through NFkB, decreases expression of adipogenic and lipogenic genes
  • inhibits LPL synthesis
20
Q

effects of TNFa on liver

A
  • increases exp of genes for fatty acid synthesis

- decreases exp of genes for fatty acid oxidation

21
Q

why are visceral adipose depots associated with more bad effects?

A

hormones secreted from visceral fat can reach liver directly through portal circulation, ask express more IL-6 and PAI-1 = increased inflammation and thrombosis

22
Q

what 2 adipokines are secreted more by subcutaneous fat?

A

leptin and adiponectin

23
Q

what are PPARs and how do they work?

A

PPARs are transcription factors involved in adipocyte differentiation and metabolism; form heterodimers with RXRs and bind to PPRE in promoter to regulate transcription

24
Q

ligands for the different isoforms

A

PPARa- fibrates
PPARg- TZDs
PPARd- fatty acids

25
Q

how are TZDs used to treat DM?

A

TZDs will promote increased fat uptake into subcutaneous fat depots which will correct the abnormal partitioning of fats into muscle and liver (seen in insulin resistance)

26
Q

describe beige adipocytes

A

at rest- act like white and store energy

with stimulation- can act like brown and dissipate energy

27
Q

what can stimulates beige adipocytes to act more like brown?

A

cold exposure
sympathetic stimulation
drugs/transcription factors

28
Q

how does thermogenesis occur in brown fat?

A

brown fat has UCP-1 present in the inner mito membrane tha uncouples the H+ gradient from ATP synthase, results in heat generation instead of ATP production

29
Q

what is lypodystrophy?

A

inability to recruit and induce terminal differentiation of pre-adipocytes that leads to little fat/fat absence

30
Q

what is the role of macrophages in adipose tissue?

A

when fat cells become too large, some will die and are then digested by macrophages. Macrophages will also regulate adipokine secretion in a paracrine manner.

31
Q

congenital generalized lipodystrophy

A

fat loss that is almost complete at birth caused by loss of function mutation in AGPAT2

32
Q

common phenotype in lipodystrophy (4)

A
  • high triglycerides
  • mild elevation in cholesterol
  • reduced HDL
  • insulin resistance
33
Q

why is insulin resistance seen in lipodystrophy?

A

since there is no adipose cell to store triglycerides, they are stored in skeletal mm (also liver)

34
Q

describe leptin levels in lipodystrophy

A

no adipose = low leptin levels that leads to hyperphagia and increased caloric intake

35
Q

what signals insulin release? amplified?

A

increased ATP/ADP ratio

amp by NADPH/a-ketoglutarate/GTP

36
Q

what can be used to gauge endogenous insulin production?

A

c-peptide level

37
Q

insulin is generally the hormone of:

A

synthesis and storage

38
Q

insulin triggers dephospho rylation which promotes-

A

anabolic processes

exception= glycolysis in skeletal mm

biochem block 3 (7 decks)

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