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BMS3052 > 23-26. Obesity, Diabetes and Nutrition > Flashcards

23-26. Obesity, Diabetes and Nutrition Flashcards

1
Q

Define

Critical race theory

A

a theoretical framework in the social sciences that examines society and culture as they relate to categorizations of race, law, and power

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2
Q

Define

Ecological Systems Theory

A

offers a framework through which community psychologists examine individuals’ relationships within communities and the wider society

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3
Q

Define

FTO gene

A

an important locus harboring common variants with an unequivocal impact on obesity predisposition and fat mass at the population level

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4
Q

Define

Genome wide association study (GWAS)

A

an approach used in genetics research to associate specific genetic variations with particular diseases. The method involves scanning the genomes from many different people and looking for genetic markers that can be used to predict the presence of a disease

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5
Q

Define

Ghrelin

A

a hormone that is produced and released mainly by the stomach with small amounts also released by the small intestine, pancreas and brain. It is termed the ‘hunger hormone’ because it stimulates appetite, increases food intake and promotes fat storage.

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6
Q

Define

Health equity

A

the notion that everyone should have a fair opportunity to attain their full health potential and that no one should be disadvantaged from achieving this potential if it can be avoided

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7
Q

Define

Hyperphagia

A

an abnormally great desire for food; excessive eating

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8
Q

Define

Hypogonadism

A

diminished functional activity of the gonads—the testes or the ovaries—that may result in diminished production of sex hormones

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9
Q

Define

Hypotonia

A

decreased muscle tone

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10
Q

Define

Leptin

A

a hormone produced by the fat cells in your body. Its main role is to regulate fat storage and how many calories you eat and burn

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11
Q

Define

Malnutrition

A

a condition that results from eating a diet in which one or more nutrients are either not enough or are too much such that the diet causes health problems

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12
Q

Define

Prader-Willi Syndrome

A

a complex genetic condition that affects many parts of the body. In infancy, this condition is characterized by weak muscle tone (hypotonia), feeding difficulties, poor growth, and delayed development

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13
Q

Define

Uniparental disomy

A

the situation in which 2 copies of a chromosome come from the same parent, instead of 1 copy coming from the mother, and 1 copy coming from the father

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14
Q

Definition

a theoretical framework in the social sciences that examines society and culture as they relate to categorizations of race, law, and power

A

Critical race theory

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15
Q

Definition

offers a framework through which community psychologists examine individuals’ relationships within communities and the wider society

A

Ecological Systems Theory

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16
Q

Definition

an important locus harboring common variants with an unequivocal impact on obesity predisposition and fat mass at the population level

A

FTO gene

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17
Q

Definition

an approach used in genetics research to associate specific genetic variations with particular diseases. The method involves scanning the genomes from many different people and looking for genetic markers that can be used to predict the presence of a disease

A

Genome wide association study (GWAS)

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18
Q

Definition

a hormone that is produced and released mainly by the stomach with small amounts also released by the small intestine, pancreas and brain. It is termed the ‘hunger hormone’ because it stimulates appetite, increases food intake and promotes fat storage.

A

Ghrelin

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19
Q

Definition

the notion that everyone should have a fair opportunity to attain their full health potential and that no one should be disadvantaged from achieving this potential if it can be avoided

A

Health equity

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20
Q

Definition

an abnormally great desire for food; excessive eating

A

Hyperphagia

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21
Q

Definition

diminished functional activity of the gonads—the testes or the ovaries—that may result in diminished production of sex hormones

A

Hypogonadism

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22
Q

Definition

decreased muscle tone

A

Hypotonia

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23
Q

Definition

a hormone produced by the fat cells in your body. Its main role is to regulate fat storage and how many calories you eat and burn

A

Leptin

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24
Q

Definition

a condition that results from eating a diet in which one or more nutrients are either not enough or are too much such that the diet causes health problems

A

Malnutrition

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25
Q

Definition

a complex genetic condition that affects many parts of the body. In infancy, this condition is characterized by weak muscle tone (hypotonia), feeding difficulties, poor growth, and delayed development

A

Prader-Willi Syndrome

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26
Q

Definition

the situation in which 2 copies of a chromosome come from the same parent, instead of 1 copy coming from the mother, and 1 copy coming from the father

A

Uniparental disomy

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27
Q

How does obesity occur?

A

Arises from energy imbalance, when energy intake is more than energy expended through physical activity

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28
Q

How is the weight status of adults typically measured?

A

Usually calculated in population surveys by measuring a person’s body mass index (BMI=weight in kg/ height2), or waist circumference

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29
Q

How is the weight status percentiles of children broken up?

A

Underweight: BMI less than 5th percentile

Healthy weight: BMI between 5th and 85th percentile

Overweight: BMI between 85‐95th percentile relative to age and sex

Obesity: BMI 95th percentile and above relating to age and sex

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30
Q

Why does childhood obesity/overweight matter?

A
  • Childhood obesity continues to be one of the most challenging public health issues of this century (WHO, 2016).
  • Associated with serious adverse short‐ and long‐term outcomes
  • Obesity‐related behaviours are established in early childhood and track through to adulthood (Han, Lawlor, & Kimm, 2010).
  • First 2000 days (conception to 5 years) are viewed as a crucial period for child obesity prevention.
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31
Q

A recent meta analysis showed children with obesity have a ______ increased risk of having obesity in adulthood

A

A recent meta‐analysis showed children with obesity have a fivefold increased risk of having obesity in adulthood

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32
Q

What are the adverse health outcomes of children with obesity?

A

“Lifestyle” health conditions such as hypertension and metabolic disorders (WHO, 2016)

Children with obesity are more likely to be admitted to hospital and have a 60% higher health care costs compared to children with healthy weight status (Hayes et al., 2016)

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33
Q

What are the implications of childhood obesity beyond physical health?

A

Negatively impacts self‐esteem and mental health

Long‐term education

Quality of life

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34
Q

Over the past decades, obesity researchers have used _______________ to summarise the complex interplay between these multidimensional contributors to excess child weight development and inform childhood obesity research and prevention strategies

A

Over the past decades, obesity researchers have used Ecological Systems Theory to summarise the complex interplay between these multidimensional contributors to excess child weight development and inform childhood obesity research and prevention strategies

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35
Q

What places parent and child factors as the most proximal influences on the development of overweight and obesity during early childhood?

A

Ecological systems theory

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36
Q

Why do high quality parent-child interactions matter to child development of obesity?

A
  • Responsive, sensitive parenting helps to build trust in the relationship and the child learns that they can rely on their caregiver to comfort them during times of distress and support their exploration of the world
  • High quality interactions impact on development of the child’s neurophysiological structures (associated with stress response, sleep, appetite) involved in supporting optimal development of self‐regulation
  • Stress response, sleep and appetite are implicated in energy regulation and eating behaviour
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37
Q

What are the child-level factors that may play a role in feeding interactions?

A

Age

Gender

Temperament

Self-regulation

Eating behaviour

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38
Q

True or False:

Excess weight is considered to be a leading cause of preventable death

A

True

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39
Q

What factors contribute to obesity?

A

Genetics/epigenetics

Lifestyle eating/exercise patterns

Socioeconomic status

Psychological factors

Cultural background

Age

Hormonal, metabolic and physiological factors

Sleep disturbances

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40
Q

True or False:

Most genetically caused obesity is monogenic

A

False

Monogenic forms of obesity are relatively rare

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41
Q

What is the heritability of BMI?

A

50-90%

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42
Q

What is the most common syndromic cause of obesity?

A

Prader-Willi Syndrome

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43
Q

What are the symptoms of Prader-Willi Syndrome?

A
  • Hypotonia: weak muscle tone, and floppiness at birth.
  • Hypogonadism: immature development of sexual organs and other sexual characteristics.
  • Obesity: caused by excessive appetite and overeating (hyperphagia), and a decreased calorific requirement owing to low energy expenditure levels, although obesity is not normally a feature of those whose food intake is strictly controlled.
  • Central nervous system and endocrine gland dysfunction: causing varying degrees of learning disability, short stature, hyperphagia, somnolence (excessive sleepiness), and poor emotional and social development.
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44
Q

What is the genetic cause of Prader-Willi?

A

Different mechanisms can lead to lack of expression of the paternal chromosome 15q11- q13 genes, hence causing PWS:

  • 65-75% cases: De novo microdeletion of this region on the paternal chromosome
  • 20-30% cases: Maternal uniparental disomy (UPD)
    1. Two maternal chromosomes, none from father
    2. Associated with advanced maternal age
  • 2-5% or fewer cases: Imprinting error epigenetic transference.
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45
Q

Levels of which hormone are increased in children with Prader Willi Syndrome?

A

Ghrelin

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46
Q

Which cell type produces leptin?

A

Fat cells

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47
Q

Double knockout of the ob gene (leptin) caused what symptoms in mice?

A

Profound obesity

Glucose intolerant/ insulin resistant

Infertile

Cold intolerant

Immune Dysfunction

No circulating leptin levels

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48
Q

What happens if a organism is unable to produce leptin?

A

Without leptin the body believes it is constantly in a state of starvation or there is an absence of fat stores.

This signals to the brain to increase food intake and reduce energy expenditure.

No satiation- patients eat uncontrollably.

Leads to profound morbid obesity.

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49
Q

How is congenital leptin deficiency in humans treated?

A

Leptin replacement therapy

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50
Q

True or False:

Individuals with leptin receptor mutations respond well to leptin replacement therapy

A

False

These individuals already have elevated circulating leptin. The issue isn’t the lack of leptin, its the inability to recognise ti

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51
Q

What is the relationship between circulating leptin and BMI?

A

As BMI increases, level of circulating leptin also increases indicating leptin resistance

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52
Q

How do we identify susceptibility genes?

A

Genome-wide association studies (GWAS)

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53
Q

What happens when FTO is over expressed in mice?

A

Increased body weight

Drastically increased fat mass

Increased food intake

Increased preference for higher calorie foods

Reduced physical active and energy expenditure

Impaired browning of white adipose tissue

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54
Q

Define

Adipokines

A

cytokines secreted by adipose tissue

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55
Q

Define

Adiponectin

A

a protein produced and secreted by fat cells that is normally abundant in the blood plasma but has reduced expression in those with obesity and insulin resistance

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56
Q

Define

Agouti-related protein (AgRP)

A

a neuropeptide produced in the brain by the AgRP/NPY neuron. It is synthesized only in neuropeptide Y (NPY)-containing cell bodies located in the ventromedial part of the arcuate nucleus in the hypothalamus. It is co-expressed with NPY and acts to increase appetite and decrease metabolism and energy expenditure

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57
Q

Define

Arcuate nucleus (ARC)

A

located around the third ventricle near the median eminence, is involved in many processes including regulating the release of hormones (eg, GnRH and prolactin) from the anterior pituitary, the LH surge, lactation, appetite and growth hormone release

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58
Q

Define

Ceramide

A

a family of waxy lipid molecules. They can participate in a variety of cellular signaling: examples include regulating differentiation, proliferation, and programmed cell death (PCD) of cells

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59
Q

Define

Cholecystokinin (CCK)

A

a hormone secreted especially by the duodenal mucosa that regulates the emptying of the gallbladder and secretion of enzymes by the pancreas and that has been found in the brain

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60
Q

Define

Diacylglyceride (DAG)

A

a glyceride consisting of two fatty acid chains covalently bonded to a glycerol molecule through ester linkages. It is able to suppress the accumulation of body fat

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61
Q

Define

Glucagon-like peptide-1 (GLP-1)

A

produced and secreted by intestinal enteroendocrine L-cells and certain neurons within the nucleus of the solitary tract in the brainstem upon food consumption. It has the ability to decrease blood sugar levels in a glucose-dependent manner by enhancing the secretion of insulin

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62
Q

Define

GLUT4

A

the insulin-regulated glucose transporter found primarily in adipose tissues and striated muscle (skeletal and cardiac)

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63
Q

Define

Insulin

A

a protein pancreatic hormone secreted by the beta cells of the islets of Langerhans that is essential especially for the metabolism of carbohydrates and the regulation of glucose levels in the blood and that when insufficiently produced results in diabetes mellitus

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64
Q

Define

Lateral hypothalamus (LH)

A

contains the primary orexinergic nucleus within the hypothalamus that widely projects throughout the nervous system;[2] this system of neurons mediates an array of cognitive and physical processes, such as promoting feeding behavior and arousal, reducing pain perception, and regulating body temperature, digestive functions, and blood pressure, among many others

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65
Q

Define

M1 macrophage

A

Classically activated, pro-inflammatory macrophages

66
Q

Define

M2 macrophage

A

Alternatively activated, anti-inflammatory macrophages

67
Q

Define

Median eminence

A

a raised area in the floor of the third ventricle of the brain produced by the infundibulum of the hypothalamus

68
Q

Define

Melanocortin 4 (MC4) receptor

A

a G protein-coupled receptor that binds α-melanocyte stimulating hormone (α-MSH). Involved in feeding behaviour, the regulation of metabolism, sexual behaviour, and male erectile function

69
Q

Define

Melanocortins

A

a group of peptide hormones which include adrenocorticotropic hormone (ACTH) and the different forms of melanocyte-stimulating hormone (MSH), and are derived from proopiomelanocortin (POMC) in the pituitary gland

70
Q

Define

Metabolic syndrome

A

a syndrome marked by the presence of usually three or more of a group of factors (such as high blood pressure, abdominal obesity, high triglyceride levels, low HDL levels, and high fasting levels of blood sugar) that are linked to increased risk of cardiovascular disease and type 2 diabetes

71
Q

Define

Neuropeptide Y (NPY)

A

a 36 amino-acid neuropeptide that is involved in various physiological and homeostatic processes in both the central and peripheral nervous systems. In the brain, it is produced in various locations including the hypothalamus, and is thought to have several functions, including: increasing food intake and storage of energy as fat

72
Q

Define

Orexigen

A

Any substance that stimulates appetite

73
Q

Define

Paraventricular nucleus (PVN)

A

a discrete band of neurons in the anterior part of the hypothalamus that produce vasopressin and especially oxytocin and that innervate the neurohypophysis

74
Q

Define

Peptide YY (PYY)

A

a short (36-amino acid) peptide released from cells in the ileum and colon in response to feeding. In the blood, gut, and other elements of periphery, it acts to reduce appetite

75
Q

Define

Pro-opiomelanocortin (POMC) neurons

A

Produces a specific type of molecule that acts as a precurosor to appetite supressor molecules

76
Q

Define

Resistin

A

an adipose-derived hormone (similar to a cytokine) whose physiologic role has been the subject of much controversy regarding its involvement with obesity and type II diabetes mellitus

77
Q

Define

Tanycytes

A

special ependymal cells found in the third ventricle of the brain, and on the floor of the fourth ventricle and have processes extending deep into the hypothalamus. It is possible that their function is to transfer chemical signals from the cerebrospinal fluid to the central nervous system

78
Q

Define

Type 2 diabetes

A

a common form of diabetes mellitus that develops especially in adults and most often in obese individuals and that is characterized by hyperglycemia resulting from impaired insulin utilization coupled with the body’s inability to compensate with increased insulin production

79
Q

Define

Vagal afferent

A

nerves that innervate the gastrointestinal tract and contain dense axonal projections and complex terminal structures that detect sensory stimuli and transmit signals towards the CNS

80
Q

Define

Ventromedial hypothalamus (VMH)

A

a distinct morphological nucleus involved in terminating hunger, fear, thermoregulation, and sexual activity.” This nuclear region is involved with the recognition of the feeling of fullness.

81
Q

Define

Visfatin

A

a protein present in several mammals, encoded by the NAMPT gene within humans, expressed to a high degree in visceral fat

82
Q

Define

α-Melanocyte-stimulating hormone (α-MSH)

A

an endogenous peptide hormone and neuropeptide of the melanocortin family. It is the most important hormone in its family responsible for pigmentation primarily of the hair and skin. It also plays a role in feeding behavior, energy homeostasis, sexual activity, and protection against ischemia and reperfusion injury

83
Q

Definition

cytokines secreted by adipose tissue

A

Adipokines

84
Q

Definition

a protein produced and secreted by fat cells that is normally abundant in the blood plasma but has reduced expression in those with obesity and insulin resistance

A

Adiponectin

85
Q

Definition

a neuropeptide produced in the brain by the AgRP/NPY neuron. It is synthesized only in neuropeptide Y (NPY)-containing cell bodies located in the ventromedial part of the arcuate nucleus in the hypothalamus. It is co-expressed with NPY and acts to increase appetite and decrease metabolism and energy expenditure

A

Agouti-related protein (AgRP)

86
Q

Definition

located around the third ventricle near the median eminence, is involved in many processes including regulating the release of hormones (eg, GnRH and prolactin) from the anterior pituitary, the LH surge, lactation, appetite and growth hormone release

A

Arcuate nucleus (ARC)

87
Q

Definition

a family of waxy lipid molecules. They can participate in a variety of cellular signaling: examples include regulating differentiation, proliferation, and programmed cell death (PCD) of cells

A

Ceramide

88
Q

Definition

a hormone secreted especially by the duodenal mucosa that regulates the emptying of the gallbladder and secretion of enzymes by the pancreas and that has been found in the brain

A

Cholecystokinin (CCK)

89
Q

Definition

a glyceride consisting of two fatty acid chains covalently bonded to a glycerol molecule through ester linkages. It is able to suppress the accumulation of body fat

A

Diacylglyceride (DAG)

90
Q

Definition

produced and secreted by intestinal enteroendocrine L-cells and certain neurons within the nucleus of the solitary tract in the brainstem upon food consumption. It has the ability to decrease blood sugar levels in a glucose-dependent manner by enhancing the secretion of insulin

A

Glucagon-like peptide-1 (GLP-1)

91
Q

Definition

the insulin-regulated glucose transporter found primarily in adipose tissues and striated muscle (skeletal and cardiac)

A

GLUT4

92
Q

Definition

a protein pancreatic hormone secreted by the beta cells of the islets of Langerhans that is essential especially for the metabolism of carbohydrates and the regulation of glucose levels in the blood and that when insufficiently produced results in diabetes mellitus

A

Insulin

93
Q

Definition

contains the primary orexinergic nucleus within the hypothalamus that widely projects throughout the nervous system;[2] this system of neurons mediates an array of cognitive and physical processes, such as promoting feeding behavior and arousal, reducing pain perception, and regulating body temperature, digestive functions, and blood pressure, among many others

A

Lateral hypothalamus (LH)

94
Q

Definition

Classically activated, pro-inflammatory macrophages

A

M1 macrophage

95
Q

Definition

Alternatively activated, anti-inflammatory macrophages

A

M2 macrophage

96
Q

Definition

a raised area in the floor of the third ventricle of the brain produced by the infundibulum of the hypothalamus

A

Median eminence

97
Q

Definition

a G protein-coupled receptor that binds α-melanocyte stimulating hormone (α-MSH). Involved in feeding behaviour, the regulation of metabolism, sexual behaviour, and male erectile function

A

Melanocortin 4 (MC4) receptor

98
Q

Definition

a group of peptide hormones which include adrenocorticotropic hormone (ACTH) and the different forms of melanocyte-stimulating hormone (MSH), and are derived from proopiomelanocortin (POMC) in the pituitary gland

A

Melanocortins

99
Q

Definition

a syndrome marked by the presence of usually three or more of a group of factors (such as high blood pressure, abdominal obesity, high triglyceride levels, low HDL levels, and high fasting levels of blood sugar) that are linked to increased risk of cardiovascular disease and type 2 diabetes

A

Metabolic syndrome

100
Q

Definition

a 36 amino-acid neuropeptide that is involved in various physiological and homeostatic processes in both the central and peripheral nervous systems. In the brain, it is produced in various locations including the hypothalamus, and is thought to have several functions, including: increasing food intake and storage of energy as fat

A

Neuropeptide Y (NPY)

101
Q

Definition

Any substance that stimulates appetite

A

Orexigen

102
Q

Definition

a discrete band of neurons in the anterior part of the hypothalamus that produce vasopressin and especially oxytocin and that innervate the neurohypophysis

A

Paraventricular nucleus (PVN)

103
Q

Definition

a short (36-amino acid) peptide released from cells in the ileum and colon in response to feeding. In the blood, gut, and other elements of periphery, it acts to reduce appetite

A

Peptide YY (PYY)

104
Q

Definition

Produces a specific type of molecule that acts as a precurosor to appetite supressor molecules

A

Pro-opiomelanocortin (POMC) neurons

105
Q

Definition

an adipose-derived hormone (similar to a cytokine) whose physiologic role has been the subject of much controversy regarding its involvement with obesity and type II diabetes mellitus

A

Resistin

106
Q

Definition

special ependymal cells found in the third ventricle of the brain, and on the floor of the fourth ventricle and have processes extending deep into the hypothalamus. It is possible that their function is to transfer chemical signals from the cerebrospinal fluid to the central nervous system

A

Tanycytes

107
Q

Definition

a common form of diabetes mellitus that develops especially in adults and most often in obese individuals and that is characterized by hyperglycemia resulting from impaired insulin utilization coupled with the body’s inability to compensate with increased insulin production

A

Type 2 diabetes

108
Q

Definition

nerves that innervate the gastrointestinal tract and contain dense axonal projections and complex terminal structures that detect sensory stimuli and transmit signals towards the CNS

A

Vagal afferent

109
Q

Definition

a distinct morphological nucleus involved in terminating hunger, fear, thermoregulation, and sexual activity.” This nuclear region is involved with the recognition of the feeling of fullness.

A

Ventromedial hypothalamus (VMH)

110
Q

Definition

a protein present in several mammals, encoded by the NAMPT gene within humans, expressed to a high degree in visceral fat

A

Visfatin

111
Q

Definition

an endogenous peptide hormone and neuropeptide of the melanocortin family. It is the most important hormone in its family responsible for pigmentation primarily of the hair and skin. It also plays a role in feeding behavior, energy homeostasis, sexual activity, and protection against ischemia and reperfusion injury

A

α-Melanocyte-stimulating hormone (α-MSH)

112
Q

What factors contribute to the development of metabolic syndrome?

A

Inflammation

Increased TAGs

Decreased HDL

Oxidative stress

Abdominal adiposity

Pro-thrombotic state

Blood glucose

Insulin resistance

Increased hypertension

113
Q

What diseases are associated with metabolic syndrome?

A

Neurological disorders

PCOS

Cancer

Cardiovascular disease

Type II diabetes

Stroke

NASH

114
Q

Which three tissues does insulin directly effect? What does it cause at these locations?

A

Liver

  • Decreased hepatic glucose production via inhibition of gluconeogenesis

Skeletal muscle

  • Increased glucose uptake (via GLUT4) - glycogen
  • Uptake of amino acids - protein synthesis

Adipose tissue

  • Increase glucose uptake (via GLUT4)
  • Inhibits lipolysis
  • Triglyceride synthesis
115
Q

Which three tissues does insulin directly effect? What does insulin resistance cause at these locations?

A

Liver

  • Increased hepatic glucose production contributes to hyperglycaemia

Skeletal muscle

  • Decreased glucose uptake cotnributes to hyperglycaemia

Adipose tissue

  • Increased lipolysis leads to increased circulating FFA
116
Q

What proportion of people with diabetes don’t know they have it?

A

1/3

117
Q

How is T2 diabetes diagnosed?

A

Fasting blood glucose (normal < 5.5 mmol/L)

Oral glucose tolerance test for people > 5.5. mmol/L (normal < 7.8 mmol/L)

118
Q

What is the heritability of T2 diabetes?

A

Having a parent with diabetes increases the risk of diabetes 2-fold, with up to 6-fold risk when both parents are affected

119
Q

T2 diabetes is characterised by defects in two areas, what are they?

A

Insulin resistance

β-cell dysfunction

120
Q

What causes β-cell failure seen in T2 diabetes?

A

β-cell compensation causing increased secretion of insulin. Exhausts cells

121
Q

Which tissue is responsible for the greatest uptake of glucose after eating?

A

Skeletal muscle

122
Q

In what four ways is diabetes also a disease of defective lipid metabolism?

A

Lipotoxicity

Inflammation (low-grade)

Altered endocrine signals

Mitochondrial dysfunction

123
Q

How do long-chain fatty acids block insulin signalling in skeletal muscle?

A

DAGs and ceramides prevent GLUT4 from reaching the cell membrane, causing decreased glucose uptake

124
Q

What causes the increase in circulating FFA in diabetes?

A

Adipocytes undergo apoptosis dues to toxicity from storing too much fat. Releases FFA into bloodstream

125
Q

What type of macrophage contributes to inflammation in obese individuals?

A

M1 macrophages

126
Q

What are the main cytokines contributing to the low-grade inflammation in obese individuals?

A

IL-6

TNFα

127
Q

What is an inflammatory hallmark of the obese state?

A

Recruitment of M1 macrophages

128
Q

How do M1 macrophages impact insulin signalling?

A

Proinflammatory cytokines impair insulin signalling. Prevents GLUT4 transportation and glucose uptake in skeletal muscle. Increases hepatic glucose production

129
Q

What effects do adipokines have on the body?

A

Energy expenditure

Food intake

Kidney function

Angiogenesis

Insulin sensitivity

Inflammation

Immunity

130
Q

What are the four major adipokines?

A

Leptin

Adiponectin

Resistin

Visfatin

131
Q

Which adipokine opposes resistin?

A

Adiponectin

132
Q

What happens to mitochondrial in diabetes?

A

Reduced number, size and activity

Reduced fatty acid oxidation proteins

Increased reactive oxygen species (ROS) - inhibit insulin signalling

133
Q

What is the main endogenous appetite stimulator?

A

Ghrelin

134
Q

What molecules inhibit appetite?

A

Leptin

Insulin

GLP-1

CCK

PYY

135
Q

What is the major site of homeostatic control of food intake?

A

Arcuate nucleus (ARC)

136
Q

What three neuropeptides are released in the arcuate nucleus neurons to control feeding?

A

POMC

  • Produced by POMC neurons
  • Precursor to melanocortins (i.e. αMSH) which inhibit FI via MC4R

NPY

  • Produced by NPY/AgRP neuron
  • Most potent orexigen; coexpressed with AgRP; acts on Y1 and Y5

AgRP

  • Produced by NPY/AgRP neuron
  • Coexpressed with NPY; antagonises αMSH
137
Q

What happens to αMSH and AgRP in a appetitde-supressing state?

A

AgRP is supressed

αMSH is released by the POMC neuron and binds to the MC4 receptor of the PVN neuron

Feeding decreased

138
Q

What happens to αMSH and AgRP in a appetitde-indicing state?

A

AgRP released by AgRP/NPY neuron

Binds to MC4 receptors and blocks action of αMSH

Feeding increases

139
Q

In what ways can NPY/AgRP neurons lead to hunger?

A

Release of:

  • NPY: acts on Y1 and Y5 receptors of PVN orexigenic neurons
  • AgRP: antagonises αMSH by binding to MC4 receptor
  • GABA: acts directly on GABA receptor located on POMC neuron inhibiting action
140
Q

What rapid signals control food intake?

A

Increased food intake:

  • NPY activating Y1 and Y5 receptors on orexigneic neurons in PVN
  • GABA inhibiting POMC neurons

Decreased food intake:

  • Glutamate activating satiety neurons in PVN
141
Q

What slow signals control food intake?

A

Increased food intake:

  • AgRP inhibits MC4 receptor of satiety neurons in PVN

Decreased food intake:

  • αMSH activates MC$ receptor of satiety neurons in PVN
142
Q

Deletion of NPY/AgRP cells leads to what?

A

Starvation and death

143
Q

Deletion of POMC cells leads to what?

A

Weight gain, obesity and glucose intolerance

144
Q

Why do endocrine hormones have an effect on the neurons of the arcuate nucleus?

A

The arcuate nucleus has a leaky blood brain barrier

145
Q

What causes the leaky BBB of the arcuate nucleus?

A

Tanycyte barrier and fenestrate cappilaries of the median eminence

146
Q

Which neurons are considered first order and which are second order?

A

First order: POMC and NPY/ArRP neurons

Second order: PVN neurons

147
Q

Which arcuate neurons do do insulin and leptin act on? What do they do?

A

AgRP/NPY:

  • Inhibit decreasing food intake

POMC

  • Activate increasing food intake
148
Q

What are the functions of ghrelin?

A

Increases food intake

Increases adiposity

Increases blood glucose

Increases growth hormone

149
Q

When is Ghrelin released?

A

During negative energy balance (fasting)

150
Q

Which ARC neurons does ghrelin act on? What does it do?

A

NPY/AgRP only

  • Activates increasing food intake
  • Also inhibits POMC neurons via GABA release
151
Q

Which part of the hypothalamus is considered the feeding center and which is the satiety center? Why?

A

Ventromedial hypothalamus

  • Satiety center
  • Lesions of VMH cause obesity

Lateral hypothalamus

  • Feeding center
  • Lesions of LH causes starvation
152
Q

What happens when you create lesions in the ventromedial hypthalamus and then later create lesions in the lateral hypothalamus?

A
  1. Lesions of VMH cause obesity
  2. Subsequent lesions of the LH reversed obesity and caused starvation
153
Q

What is the dual center hypotheisis of feeding?

A
154
Q

Which other section of the hypthalamus does leptin act? What does it do?

A

Ventromedial hypothalamus

Alters BDNF reducing food intake

155
Q

Where do orexin and melanin act to increase food intake?

A

Lateral hypothalamus

156
Q

Which molecule(s) inhibit orexin and melanin to reduce food intake?

A

Melanocortins (e.g. αMSH)

157
Q

Where does ghrelin act to increase food intake?

A

NPY/AgRP neurons of ARC

158
Q

Where does PYY act to decrease food intake?

A

Brainstem (vagal afferents)

Area postrema

Arcuate nucleus

159
Q

Where does GLP-1 act to decrease food intake?

A

Brainstem (vagal afferents)

Area postrema

Arcuate nucleus

160
Q

Where does CCK act to decrease food intake?

A

Brainstem (vagal afferents)

161
Q

How does GLP-1 inhibit food intake?

A

Vagal afferent connection

Inhibits food intake via GLP1-R

Acts directly on POMC neurons

Indirectly inhibits NPY/AgRP neurons via GABA

162
Q

How does PYY inhibit food intake?

A

Inhibits food intake via Y2 receptors on NPY/AgRP neurons

Inhibits release of NPY/AgRP

BMS3052 (26 decks)

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