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NUTR 301 > Lecture 5 Energy Balance & Obesity > Flashcards

Lecture 5 Energy Balance & Obesity Flashcards

1
Q

How is energy balance regulated?

A

CNS is the controller which receives input from peptides, hormones and vagal afferents and the output from the CNS is changes in food intake and energy expenditure resulting in system energy balance

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2
Q

What is the CNS integration of afferent signals?

A
  • short term signals - meal
  • long term signals - adipose tissue storage
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3
Q

What helps to integrate afferent signals from the CNS?

A

numerous neurotransmitters and neuropeptide systems

redundancy to maintain energy balance

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4
Q

What is the efferent response of food intake?

A

regulate the level of
* appetite
* energy expenditure (activity)
* nutrient partitioning
* reproduction and growth
* hormones

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5
Q

What are the afferent neurotransmitter signals controlling energy balance?

A
  • Meal: glucose, aa, fatty acids
  • Adipose: leptin
  • Pancreas: Insulin, amylin, PP
  • Stomach: Ghrelin
  • SI: CCK, PYY, GLP-1, OXM
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6
Q

Integration of meal related CNS signals in physiological control of food intake

A

Short-acting
* quantity and quality of food
* The hypothalamus is sensitive to blood concentrations of glucose, aa, and fatty acids
* Mostly negative feedback/inhibitory

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7
Q

Integration of gut signals in physiological control of food intake

A

mechanical (stretch receptors) and chemical (peptides from GI tract)
* GI-tract receptors act in combination to reduce meal size and lengthen inter-meal satiety

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8
Q

Integration of neuron information in physiological control of food intake

A

Neuron information is collated by brain stem NTS and is sent onto the hypothalamus.

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9
Q

Gut peptides that reduce meal size vs. increase meal size

A

Reduce:
* Cholecystokinin
* Bombesin family (BBS, GRP, NMP)
* Glucagon
* Glucagon-like peptide 1, gulcagon-like peptide 2
* Amylin
* Somatostatin
* Enterostatin
* Apolipoprotein A-IV
* Gastric inhibitory peptide

Increase:
* Ghrelin

Most GI peptides involve inhibition

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10
Q

Role of

CCK

A

Cholecystokinin - SI Duodenum
* Gall bladder contraction
* Gastrointestinal motility
* Pancreatic exocrine secretion

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11
Q

Role of

Secretin

A

SI Duodenum S cells
* Gall bladder contraction
* Gastrointestinal motility
* Pancreatic exocrine secretion

responds to acidic chyme

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12
Q

Role of

GIP

A

Gastric inhibitory polypeptide: stomach & SI Duodenum
* Incretin activity

Stimulate decrease in blood glucose levels by releasing insulin

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13
Q

Role of

Motilin

A

SI-Duodenum
* Gastrointestinal motility

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14
Q

Role of

Ghrelin

A

Stomach
* Hunger
* Growth Hormone release

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15
Q

Role of

Gastrin

A

Stomach
* Acid secretion

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16
Q

Role of

Insulin & glucagon

A

Pancreas
* glucose homeostasis

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17
Q

Role of

pancreatic polypeptide

A

pnacreas
* gastric motility
* satiation

18
Q

Role of

Amylin

A

pancreas
* glucose homeostasis
* gastric motility

19
Q

role of

GLP-1

A

Glucagon-like peptide 1: LI
* Incretin activity
* satiation

20
Q

Role of

GLP-2

A

Glucagon-like peptide-2: LI
* GI motility and growth

21
Q

Role of

Oxyntomodulin

A

LI
* satiation
* acid secretion

22
Q

Role of

PYY

A

peptide tyrosine tyrosine - LI ileum and colon
* satiation by slowing gastric emptying

23
Q

What are the long term signals for integration of food intake?

A

Long term signals from fat storage and appetite signals the CNS hunger/ food intake need.
* Includes the peptides leptin and insulin.

24
Q

Role of

Leptin

A

secreted by adipocytes proportional to size of fat stores
* reduces foot intake
* elevates EE

25
Q

Role of

Insulin

A

secreted by B-cells in pancreas and reflect fuel availabilty
* glucose uptake by cells
* reduction in appetite

26
Q

Insulin resistant

A

Lack of sensitivity to insulin, more secreted for same effect

27
Q

How does the CNS converge information?

A
  • short term meal derived signals collated by the NTS in the brainstem
  • short and long term signals collated by paraventricular nucleus (PVN) located in the ventromedial hypothalamus
  • Lateral hypothalamus (LH); stimulates feeding
  • Arc in hypothalamus converges adiposity signals
28
Q

How do insulin and leptin act on the brain to regulate food intake with energy surplus?

A

Increased hormone secretion converges at the Arc and inhibits food intake and increases EE
* inhibits NPY and AgRP neurons in ARC thus inhibiting orexigenic (LHA) neurons in stimulation from NPY and preventing anorexigenic (PVN) neuron inhibition from AgRP.
* Stimulates POMC neurons in the ARC which stimulates aMSH which stimulate anorexigenic neurons (PVN)

29
Q

How do insulin and leptin act on the brain to regulate food intake with energy deficit?

A

Decreased hormone secretion converges at the Arc and stimualtes food intake and decreases EE
* NPY and AgRP neurons in ARC are stimulated thus orexigenic (LHA) neurons are stimulated from increased NPY and anorexigenic (PVN) neurons are inhibited from increased AgRP.
* Inhibites POMC neurons in the ARC which inhibits aMSH which cannot act on anorexigenic neurons (PVN), thus inhibting them

30
Q

How do efferent signals control energy balance?

A

Long term signals
* Energy deficit promotes feeding and energy storage via PNS (vagus nervue)
* Excess energy promotes satiety and EE vis SNS and adrenal medulla

31
Q

How do the efferent signals from energy deficit promote energy storage?

A
  • stimulates the secretion of digestive enzymes
  • stimulates intestinal motility and peristalsis
  • relaxes intestinal sphincters
  • Increases insulin release
  • Increases adipose tissue insulin sensitivity
  • Increases substrate partitioning into adipose tissue
32
Q

How do the efferent signals from excess energy promote EE?

A
  • Increases adaptive thermogenesis by BAT
  • Increases movement
  • Inhibits insulin release and promotes insulin sensitivity
  • Increases glycogenolysis and fatty acid oxidation in skeletal muscle
  • Increases lipolysis in adipose tissue
33
Q

What is eating?

A

A behaviour controlled by the brain

34
Q

homeostatic vs. hedonic control of eating

A

appetite ≠ hunger
environmental and genetic influences can override physiological feedback loops that control set point.

35
Q

Role of epigenetics in energy balance

A

interaction of genes and the environment cause changes that effect the way your genes work by changing how your body reads a DNA sequence

36
Q

What does obesity reflect?

A

Reflects an imbalance between energy uptake and expenditure that is mediated by behaviour and is excess of adipose tissue accumulation

37
Q

Classifications of obesity based on BMI

A
38
Q

Health risks associated with obesity

A
  • Type 2 diabetes
  • Dyslipidemia
  • High blood pressure
  • Metabolic syndrome
39
Q

Medical complications of obesity

A
  • Pulmonary disease
  • Nonalcoholic fatty liver disease
  • Gall bladder disease
  • Gynecologic abnormalities
  • Osteoarthritis
  • Skin problems
  • Gout
  • Idiopathic intracranial hypertension
  • Stroke
  • Cataracts
  • Coronary heart disease
  • Diabetes
  • dyslipidemia
  • hypertension
  • Severe pancreatitis
  • Cancer Phlebitis
40
Q

What is metabolic syndrome

A

A cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes:
* increased waist circumference
* BMI >30
* increased triacylgyceride level
* decreased HDL-C
* Increased BP
* Increased glucose levels

41
Q

Treatment for obesity

A
  • Prevention with regulating energy intake
  • Manage weight loss
  • Lifestyle changes
  • Anti-obesity drugs
  • Surgery

NUTR 301 (32 decks)

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