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OBESITY AND WEIGHTLOSS > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

What are the symptoms of MS?

A

Central obesity, high BP and triglycerides, low HDL-Cholesterol, and insulin resistance

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2
Q

What is the prevalence of MS in people over 30 in Western countries?

A

10-20%

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3
Q

What is the prevalence of MS in people over 30 in Western USA?

A

25%

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4
Q

What is the most popular application of Nutri-sciene?

A

prevention and management of metabolic syndrome

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5
Q

What is the difference in obesity in woman from men?

A

Estrogen levels keep woman from becoming obese, whereas men are more inclined to obesity way before.
When there is too much glucose in the blood over a period of time, the pancreas is in overdrive

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6
Q

What is resting metabolic rate dependent on?

A

caloric need and intake and how much muscles you have

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7
Q

how does sugar make you gain weight?

A

In Metabolic syndrome glucose levels are higher, muscles are insulin resistant. High levels of sugar in the blood make you more hungry because it makes you more sensitive to sugar levels in the body which will make you gain weight

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8
Q

What are the benefits of Turmeric?

A

Turmeric is powerful anti-oxidant, natural antibiotic and anti-inflammatory.
Also increases sensitivity to insulin so you absorb more glucose. You think you would gain more weight, but it actually suppresses hunger and you get full quicker off of smaller food portions

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9
Q

What were the results of the Experimental study in mice Low-fat diet; High-fat diet; High-fat diet + Curcumin?

A

After 26 weeks of High-fat diet + curcumin the glucose sensitivity was the same as in low-fat group = no weight gain, and do not develop liver steatosis
In High-Fat group alone, a full-blown metabolic syndrome at the same time point (26 weeks) = obesity

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10
Q

What is liver steatosis?

A

fat stored in the liver which is not good for the liver because it compromised, and the body isn’t able to compensate when the sugar drops since the liver isn’t functioning as normal

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11
Q

What is functional foods?

A

food that contains physiologically active substances actively contributing to the promotion of health

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12
Q

What are nutraceutical components?

A

Physiologically active substances extracted from functional foods or non-edible plants/animals. Nutraceuticals have therapeutic or disease preventive effects

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13
Q

What are the benefits of Coffee?

A
  1. prevents alcoholic liver cirrhosis
  2. a skin cream spiked with caffeine lowers the risk of skin cancer in mice.
  3. increase attention and memory performance
    decrease risk of heart (Caffeine builds resistance to the extent that people start to have lower blood pressure over time)
  4. liver disease
  5. increase physical performance and muscular recovery
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14
Q

What is an antioxidant?

A

An antioxidant is a substance that suppresses cell damage caused by oxidation due to free radicals, and are biosynthesized by plants to helps us with damage coming from free radicals

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15
Q

How does free radicals affect our cells?

A

oxidative stress (free radicals) breakdown your cell, causing premature aging and disease

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16
Q

What is epidemiology?

A

study of how a disease or other health attribute is distributed in populations and what factors influence or determine this distribution.

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17
Q

What are the behaviors leading to chronic diseases?

A

(smoking, alcohol, unhealthy diets, lack of exercise) accounts for 800,000 death in US annually

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18
Q

What is the difference between pear and apple shape?

A

Pear shape/ghneoid – female, under control of estrogen. More fat stored on the outside of the body cavity
Apple shape – majority of fat is visceral fat around the midsection providing easy access to pre-inflammatory substances to the liver leading to liver steatosis

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19
Q

What ways can you measure obesity?

A

BMI and excess body fat
Obesity Class I: 30 - 34.9
Obesity Class II: 35 - 39.9
Extreme Obesity: >40

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20
Q

What percent of people are overweight?

A

males - 71, females - 62

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21
Q

What percent of people are obese?

A

males - 31, females - 33

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22
Q

What percent of people are severely obese?

A

males - 3, females - 7

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23
Q

What is the obesity paradox?

A

countries with less GDP tend to gain obesity faster. Economic burden of obesity and its complications is shifting rapidly towards the poor.

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24
Q

What are the BMI for evaluating obesity in children?

A

BMI between 5th & <85th percentile: Healthy weight
BMI between 85th & 95th percentile: Overweight
BMI >95th percentile: Obese

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25
Q

What is the Bigger 10-year-old?

A

The avg. 10 year old American boy around the turn of the millennium was more than 14 lbs. heavier than the average boy of the same age in the early 1960’s, while the difference in heigh is just over an inch

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26
Q

Etiology of childhood obesity

A

genetics: Low Metabolism, Poor Appetite Control, Low Fat Free Mass, Low Levels of, Lipid Oxidation Rate

Environment: Sedentary Lifestyle, and Access to Food

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27
Q

What are the Gender differences in obesity?

A

Increased risk for health problems: Women with > 35% body fat (ideal–20-35%)
Men with > 25% body fat (ideal 8-25%)

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28
Q

What promotes apple shame?

A

Abdominal fat drains by blood directly into the Liver Promoted by testosterone and alcohol intake

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29
Q

What are the waist measurements of apple shape?

A

> 40” for men

> 35” for women

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30
Q

What is the deceases of the capillaries caused by diabetes?

A

retinopathy, nephropathy, Neuropathy

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31
Q

What is the deceases of the arteries caused by diabetes?

A

coronary and cerebrovascular disease - diabetic patients have an increase 2-4 folds increase risk of developing heart disease and stroke, and 75% will have hypertension

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32
Q

What vessels suffer in obesity?

A

Insulin resistance tends to develop faster in obesity leading to high amounts of glucose in the blood over a longer period of time. The first vessels to suffer are capillaries because the speed of blood flow is slowest in the capillaries. Whenever we have damage o the blood vessel, we have tissue hypoxia and damage to the tissue

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33
Q

What are the medical complication of obesity?

A

stroke, cataracts, osteoarthritis, gout, venous stasis, pancreatitis, gallbladder problems

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34
Q

What are the cardio complications of obesity?

A

Diabetes, Dyslipidemia (change ratio of excess lipids in the blood), Hypertension

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35
Q

What cancers are caused from obesity?

A

breast, uterus, cervix, colon, esophagus, pancreas, kidney, prostate

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36
Q

What are the GYN complications of obesity?

A

abnormal menses, infertility, PCOS

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37
Q

What are the NAFLD complications of obesity?

A

steatosis, steatohepatitis, fibrosis and cirrhosis

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38
Q

What are the Pulmonary complications of obesity?

A

Shortness of breath, obstructive sleep apnea, chronic hypoxic states

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39
Q

What is the study with underweight individuals and mortality?

A

People who are underweight have an increase probability of death that is substantially higher than those or normal weight

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40
Q

What is type 2 diabetes?

A

the pancreas is functioning normally, but there’s an insulin resistance.
Younger people are getting it now (between 10-19 years)
Non-insulin-dependent diabetes mellitus (NIDDM)
Adult-onset diabetes
Associated with obesity

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41
Q

What is the number of Obesity-related deaths?

A

Obesity and overweight account for more than 300,000 premature deaths annually in US, only tobacco-related deaths outrun obesity.
Obesity would surpass tobacco as the leading cause of death worldwide in the next decade

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42
Q

What is type 1 diabetes?

A

Insulin-dependent diabetes mellitus (IDDM)
Juvenile-onset diabetes
treates with insulin

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43
Q

What is the normal plasma glucose levels?

A

3.9-8.3 mM

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44
Q

What hormones increases plasma glucose levels?

A

Glucagon, Epinephrine, Cortisol, Growth hormone

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45
Q

What is Spohn?

A

drinking gallons of water a day in order to dilute high levels of glucose in the blood

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46
Q

What is cellular caramelization?

A

Caramelization (Millard rxn), driven by glucose only occurs in the presence of glucose, And in diabetes, our cells are camerlizing faster because of this excess glucose

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47
Q

What is the result of Mailard reactions?

A

Maillard reaction results in premature aging.

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48
Q

What results from glycerlation/HbA1C?

A

if blood sugar remains elevated for prolonged periods in poorly controlled diabetes increases glycation and AGE formation goes up 4x increasing premature onsets of a wide range of age-related complications

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49
Q

What are the 2 blood test for diagnosis of diabetes?

A

fasting glucose and oral glucose tolerance test

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50
Q

What is OGTT?

A

OGTT also referred to as the glucose tolerance test, measures the body’s ability to metabolize glucose, or clear it out of the bloodstream.

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51
Q

What is HOMA Scores?

A

Homeostatic model assessment (HOMA) was first used in 1985 and was derived mathematically by looking at the interaction between β-cell function and insulin resistance of normoglycemic patients.
HOMA > 2.2 is a cut-off for insulin resistance; increases as we progress in life

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52
Q

What are the Anti-diabetic medications (non-insulin)?

A
  1. Reduce glucose production by the liver (metformin)
  2. Slow the absorption of carbohydrates from the small intestine (acarbose, α-glicosidase inhibitor)
  3. Increase insulin production by the pancreas (sulfonurea)
  4. Increase the insulin sensitivity of cells (TZDs)
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53
Q

What is snoring?

A

hypoxia of the brain which ultimately lead to stroke

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54
Q

What are the results of the diabetes prevention program?

A

Lifestyle modification is more efficient than metformin

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55
Q

What is Metaformin?

A

helps people stay on diet by decreasing hunger, and less snacking, and it also decreases insulin resistance

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56
Q

How does obesity cause cardiovascular disease?

A

Obesity predisposes people to increase blood clots and cholesterol plaque, making it an independent risk for cardiovascular disease

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57
Q

What is hypertension?

A

blood vessels are too rigid and they cannot relax when they contract. Because of this rigidity, the heart wears with every heart beat

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58
Q

What is coronary heart disease?

A

It is the most common type of heart disease.
Hardening and narrowing of the coronary arteries, that supply blood to the heart muscle due the plaque buildup, reducing the flow of blood and oxygen to the heart.
CHD can weaken the heart muscle and lead to heart failure.
29% of deaths in the US

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59
Q

What are the factors the increase the risk of heart disease and attack?

A

1) Tobacco Smoke
2) High Blood Cholesterol
3) High Blood Pressure
4) Physical Inactivity
5) Obesity and Overweight
6) Diabetes Mellitus
7) Stress
8) Alcohol
9) Diet and Nutrition
10) Age

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60
Q

What is the obesity paradox?

A

Underweight and normal weight patients had 3.6 and 2.1 times (60%) higher risk of death than overweight or obese CHD patients.
Overweight and obesity predict better survival in pts with stable CHD.

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61
Q

What is he 2-hit model of NASH?

A

INSULIN RESISTANCE is the “first hit“ that sensitizes the liver to potential “second hits” resulting in NASH.
“Second hit” (OXIDATIVE STRESS ) was further substituted with multiple hits involving endogenous and exogenous stress factors

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62
Q

How is Hep C drug resistance shown in obese individuals?

A

Patients on hep C therapy typically develop anemia, depression (because drug treatment causes depression in the patients). Diabetes somehow helps the virus to resist the treatment for Hep C. People infected with some genotypes of Hep C virus are pushing patients to develop diabetes

63
Q

What is Polycystic ovary disease?

A

Development of cyst instead of eggs, so there is no oocyte. Can be caused by progesterone/estrogen imbalance, or excess testosterone

64
Q

What is the Prevalence of Nonalcoholic Fatty Liver Disease in Women With Polycystic Ovary Syndrome?

A

Fatty liver was identified in 55% of subjects with PCOS, nearly 40% of whom were lean women.

65
Q

What is the Treatment for PCOS?

A

Exercise, healthy diet and weight control, Diabetes medication metformin (Glucophage)

66
Q

How does Metformin work?

A

Metformin stimulates glucose uptake by muscles and suppresses glucose release by liver

67
Q

How does Metformin operate in PCOS and diabetes?

A

Metformin therapy decreases both Androgen production

and Hyperinsulinemia in women with PCOS

68
Q

What is the Cycle of PCOS?

A

PCOS increases insulin resistance, which then in turn elevates testosterone and estrogen, decreases sex-binding globulin and increases androstenedione and DHEA

69
Q

What is sleep apnea?

A

Sleep disorder with abnormal pauses in breathing, causing intermittent hypoxia. Each pause in breathing can last from a few seconds to minutes, and may occur 5 to 30 times or more an hour

70
Q

What causes sleep apnea?

A

occurs when the upper airway collapses, and this can cause a lack of oxygen supply to the brain. LOUD SNORING IS A SYMPTOM

71
Q

What is silent strokes?

A

Silent stroke is linked with sleep apnea due to a lack of O2 to the brain. The presence of silent infarcts more than doubles the risk of subsequent stroke and dementia. Having multiple silent strokes is linked with memory loss, difficulties with walking and mood problems.

72
Q

What is the treatment of obstructive sleep apnea?

A

continuous positive airway pressure (CPAP device)

73
Q

What role does obesity play in Arthritis?

A

For obese and overweight patients, there is a dramatically increased force on the joints, leading to unconscious drive to restrict activities “Inflammatory side” of Arthritis also is aggravated by obesity (1 in 3)

74
Q

What is depression?

A

a mood disorder in which feelings of sadness, loss, anger, or frustration interfere with everyday life for weeks or longer

75
Q

How are Depression and obseity related?

A

High BMI = high prevalence of depression

76
Q

What is Stress?

A

STRESS is key contributor to both obesity and depression

77
Q

What is the macrophage theory of depression?

A

Inflammatory stimuli cause both sickness behavior and depression-like behavior
Chronic immune activation is common in depression AND depression-associated conditions such as Hep C, aging and somatic disorders

78
Q

How does Anti-depression medication affect obesity?

A

stimulate weight gain by increasing appetite and reducing motor activity causing even more obesity

79
Q

What are the most prominent cancers caused by obesity in men and woman?

A

men - liver, esophageal and pancreatic cancer are most prominent
woman - uterine, kidney, and cervical cancer are most prominent

80
Q

How does obesity cause cancer cell proliferation?

A

A. Insulin has mitogenic effects
B. Insulin signaling inhibitors are suppressed (insulin-like growth factor binding protein 1/IGFBP-1 and IGFBP-2)
bio-availability of IGF1 is increased
C. IGF-1 promotes cellular proliferation and inhibits apoptosis through its receptor in several tissues.
D. Additionally, less SHBG (steroid hormone binding protein) is made by liver –> more free sex steroids are available for direct carcinogenic action

81
Q

How does IGF-1 work?

A

Insulin and IGF1 signal through the insulin receptors (IRs) and IGF1 receptor (IGF1R), respectively, to promote cellular proliferation and inhibit apoptosis in many tissue types.

82
Q

What is the Mitogenic effects of insulin?

A

Decrease insulin resistance will decrease insulin like growth factor, and thus decrease/slow down tumor growth in cancer patients

83
Q

What are the Sex steroid hormone and pro-carcinogenic effects of obesity?

A

A. Adipose tissue produces the enzymes aromatase and 17ß-hydroxysteroid dehydrogenase 17B-HSD
B. Aromatase converts the androgens δ4-androstenedione and testosterone (T) into the estrogens estrone (E1) and estradiol (E2)
C. 17ß-HSD converts less biologically active hormones δ4A and E1 into the more active hormones T and E2, respectively.
D. MORE ADIPOSE = MORE ESTROGENS!
E. Which means Less SHBG made by liver = more FREE SEX STEROIDS contributing to cancer

84
Q

What is the purpose of Progesterone?

A

Progesterone counter-balances levels of estrogen. Men do not have estrogen supply from the uterus, so an increase in fat will increase estrogen production, and no progesterone to counterbalance it, contributing to increase cancer risk and replication

85
Q

What is the realtionship between Endometrial carcinoma and obesity?

A

Number 1 cancer in obese females
The more children a woman has, the less of a risk she has of developing endometrial carcinoma; likewise for oral contraceptives

86
Q

What is the realtionship between Prostate cancer and obesity ?

A

Prostate produces specific cells, which gets diluted in the body; the bigger you are, the more diluted these components making it hard to measure pancreatic cancer, and thus a lowe PSA reading in obese men

87
Q

What is the realtionship between Breast carcinoma and obesity?

A

Higher breast carcinoma in obese men then overweight men due to increase amounts of estrogen production do to increase amounts of adipose cells, and the increase size of the breast tissue due to obesity because there is more availability of cells to for the cancer to mutate

88
Q

What was the outcome of the twin studies?

A

obesity is greater concordance among MZ twins compared to DZ twins

89
Q

What is the conclusion of obesity and adoption study?

A

genetic influences have an important role in determining human fatness in adults, whereas the family environment alone has no apparent effect. The incidence of obesity is high in biological relatives then adoptive

90
Q

What are the 2 kinds of obesity?

A

monogenic and polygenic

91
Q

What is manogenic and polygenic?

A 
Monogenic – genes are faulty, but the patient cannot escape. They can try to diet, but it will never bring the patient back to the normal weight class
Polygenic – when you are predisposed obesity via our environment, but our genes help maintain us to not be obese, and vise versa
92
Q

What is the anorexigenic signal?

A

Suppress food intake and Increase energy expenditure
Pro-opiomelanocortin (POMC)
Cocaine- and amphetamine-regulated transcript (CART)

93
Q

What is the orexigenic signal?

A 
Stimulate food intake and Decrease energy expenditure
Neuropeptide Y (NPY)
Agouti-related protein (AGRP)
94
Q

What is the lipostatic theory?

A

Decrease in body fat will send signal to the brain to increase adipocytes to get us back to our stable weight;
trying to gain weight is difficult, and Trying to lose weight is also difficult
*Homeostasis—– very difficult to get from stable obesity back to a norm (Hormone that’s doing this is found in adipose tissue)

95
Q

How does leptin work?

A

Leptin in the thalamus where it is increase anorexigenic signals, so CART and POMC and decrease orexigenic signal = decrease of appetite leasing to lower fat which will neg.feedback to lower leptin and unbind it from the receptor in the brain, reducing metabolism and stimulating appetite and increasing fat once again

96
Q

How does Leptin signaling work?

A

Once leptin binds to its receptor, it activates JAK/STAT pathways, which subsequently turn some genes on/off

97
Q

What else does leptin regulate?

A

puberty, loss of bone density in old age, stimulation of liver fibrosis and congenital obesity

98
Q

What is the leptin gene mutation?

A

Human heterozygotes for the G133 mutation in the leptin gene have low serum leptin levels and increased body-fat percentage relative to controls.
Can be treated with external leptin injection, but only short-term b/c the body will reject it like an antigen since they never had the gene to begin with

99
Q

Why can’t obese individuals be treated with leptin?

A

obese people already have a lot of leptin and are perhaps leptin resistant

100
Q

What is the mechanistic basis of leptin resistance in obese individuals?

A
  1. RECEPTOR PROBLEMS: Mutations of LepR (VERY RARE!) or decrease in receptors for leptin in the brain
  2. Reduced TRANSPORT of the leptin through BLOOD-BRAIN BARRIER
    (high levels of fats in the blood disrupt transport through BBB)
  3. Feedback inhibition of leptin receptor by SOCS3: (SOCS3 is stimulated by leptin, in turn, binds to leptin receptor and shuts it off)
  4. Increase in PTP1B phosphatase shuts off signals downstream of LepR (PTP1B removes phosphates from JAK2 and leptin receptor and shuts it off)
101
Q

What are the symptoms of Bardet-Biedle Syndrome?

A

Early blindness, Kidney cysts, Polydactily (extra digits), Obesity, Hypogonadism, Dev. delays/ mental retardation

102
Q

BBS = primary cilia dysfunction

A

Dysfunction in cilia is caused by BBS and contributes to to adipose
BBS prevent things from getting to the tip of cilia and binds to the top
Causes early blindness and kidney failure

103
Q

What is ther ealtionship between cilia and BBS?

A

LEPTIN RECEPTOR is located in cilia on POMC neurons
BBS proteins deliver leptin receptor up the cilia
BBS patients are deficient in LEPTIN SIGNALING causing individual to eat more

104
Q

What is the MC4-R mutation (Melanocortin)?

A

most common known monogenic cause of human obesity, rending MC4-R insensitive to MSH (anorexigenic hormone) predisposing people to obesity from infancy
>4% morbidly obese children have a mutation in one MC4-R allele (Haploinsufficiency-lacking cope of a gene; dominant mutation; double mutants also found)

105
Q

What is the PMOC Gene mutation?

A

mutations in human POMC (where MC1-5R binds) with recessive pattern of inheritance
- red hair (MC1-R), hyperphagia and obesity (MC3-4)

106
Q

What is the antagonist of melanocortin?

A

α-melanocyte-stimulating hormone (α-MSH) anorexigenic signal Cleaved from precursor molecule POMC, Binds to melanocortin receptors
Agouti-related protein (human) = orexigenic signal Homologous to agouti protein in mouse. Antagonist of the melanocortin receptor

107
Q

What is leptin?

A

leptin produced by the hypothalamus, increases the anorexigenic signals.
it is needed for children to go through puberty

108
Q

What is the role of agouty protein?

A

Agouty protein produced ectopically in Agouty mice:
in skin gives a yellow coat color; in brain, gives obesity
Action of Agouty protein is reversible by extraneous addition of POMC encoded peptide α-MSH

109
Q

What was the conclusion of the studies of monogenic obesity?

A

As of now, obesity due to genetic changes is due to
Defect is in the satiety centers in the brain (hypophasgia and loss of control of appetite not due to slow metabolism)
Affects appetite control centers in the brain, thus Obesity is not due to ‘slow metabolism’.

110
Q

What is Polymorphism?

A

In Genetics, a polymorphism can be defined as a sequence variant that has an allele frequency of greater than 1% in the population

111
Q

What is the difference between a mutation and polymorphism?

A

Opposition to polymorphism Is a mutation. Mutation influences our phenotype, whereas polymorphism doesn’t

112
Q

What is the difference between synonymous and non-synonymous coding of SNPs?

A

Synonymous: when single base substitutions do not cause a change in the resultant amino acid
Non-synonymous: when single base substitutions cause a change in the resultant amino acid, influencing gene expression by regulation

113
Q

What is the thrifty gene Theory?

A

“thrifty” genes initially selected to conserve glycogen stores by oxidizing greater quantities of fatty acids to maximize survival during famine and exercise. Those with Thrifty genotypes gain weight under modern conditions

114
Q

What are the problems with the thrifty gene hypothesis?

A

assumes its advantageous to store fat rather then glycogen, and inability to adapt once food no longer scares, and predicts obesity being genetic

115
Q

What candidates influence obesity?

A
  1. Morbide obesity
  2. Life span
  3. Weight gain
  4. Obesity onset
  5. Fat mass
  6. Glucose levels
  7. Lipid levels
  8. Food intake
  9. Physical activity
116
Q

What is FTO GENE?

A

Fat mass and obesity-associated transcript individuals with two copies of the obesity-risk FTO variant are biologically programmed to eat more. on average, people with both FTO and new MC4R variants are 3.8 kg (8.5 lb) heavier.

117
Q

How is FTO expressed?

A

FTO gene is expressed in arcuate nucleus (same place where leptin and POMC act) . Expression of FTO gene is increased when animals fed high-fat diet, and in individuals with 2 copies of the gene

118
Q

What is RPGRIP1L?

A

RPGRIP1L localizes in the primary cilia and centrosomes of ciliated cells and is very closely related to FTO

119
Q

What is the difference between nulli/primiparous?

A

Nulliparous – having no children

Primiparous – having one child

120
Q

What is the depression odds ratio?

A

0.92

60% of most European populations are carriers of the A “risk” allele; 17% in some Asian populations

121
Q

What is cachexia?

A

wasting as seen in cancer patients

122
Q

How many percent of men diet?

A

25 (woman - 40)

123
Q

Why is dieting inefficient?

A

Dieting has 95% long term failure rate and Often results in higher weight than before the diet

124
Q

Why do diets fail?

A
  • Weight loss is often water loss
  • Supplements may be not working or dangerous
  • Diet may lack essential nutrients
  • Metabolism may slow down if caloric intake is low.
  • Most (if not all) diets simply are not sustainable long term
125
Q

What is a calorie?

A

how much energy you need to increase the temperature of 1 kilogram (about 1 L*) of water by 1˚C.

126
Q

Why is crash dieting not efficient?

A

Body goes into energetic saving mode when you starve yourself due to the lack of nutrition, and basal metabolism goes down

127
Q

What are the major types of bariatric surgery?

A

gastric band, and gastric bypass (more efficient), sleeve

128
Q

What is gastric band?

A

For patients with BMI <45, quick recovery and short hospital state, reversible, avg. weight loss 50%

129
Q

What is gastric bypass?

A

avg. weight loss 70%, 6 weeks recovery and 6 nights stay, improves metabolic and hepatic abnormalities associated with NAFLD

130
Q

What is (1930) Ampheatmines?

A

Suppress appetite and increase alertness, making people more energetic and more likely to burn calories. in 1960, people began mixing with TH and laxatives which caused addiction and high BP and CO

131
Q

What is Ephedrine?

A

obesity med that is a weaker analogy to meth with very similar structure and action as amphetamine derived from plant Ephedra

132
Q

How does Ephedrine work?

A

dopamine re-uptake inhibitor which will then increase sympathetics efferent leading to increase thermogenesis and metabolism

133
Q

How does Amphetamines act?

A

inhibits domaine re-uptake (b/c obese people have fewer dopamine receptors) + enhances dopamine release –> increase dopamine signaling and decreasing fatty and sweet food cravings

134
Q

How for Fen-Phen work?

A

Increases dopamine and serotonin, and the person feels very happy. They forget to eat and they don’t have food cravings b/c it induced feeling of being full

135
Q

What is Fen-Phen?

A

it’s a combination of Meth + Ecstasy

136
Q

Why was Fen-Phen removed from the market?

A

Heart valves contain serotonin receptors. When stimulated, they provide growth signal. This improper growth leads to valve thickening. Valve becomes inefficient (30-2%) and blood leaks back into the heart. The chambers of the heart become overloaded with blood, enlarging the heart and impairing its ability to send blood throughout the body.

137
Q

How does Sibutramine (meridia) work?

A

its selective serotonin and noradrenaline re-uptake inhibitor, like Fenfluramine (Fen) but not as efficent; it is an analogue of meth. it decreases weight, glucose metabolism and inflammation, but increase sympathetics

138
Q

How does Xenical (roche)/Alli work?

A

Works in the gut. We ingest dietary fats that are converted from tri to monoglycerides via pancreatic lipase and absorbed into the s.intestines. What the drug did was to affect the pancreatic lipase so the majority of fat (30%) will not be broken down and absorbed

139
Q

What is the outcome of 4-years on Orlistat?

A

A 37% reduction in risk of development diabetes type 2

side-effects were fatty stool

140
Q

What is the new criteria since 2012 for FDA to approve anti-medication drug?

A

35% of treated persons must lose at least 5% of their body weight, and that group should include at least twice as many individuals as the number of patients who achieve a similar weight loss on placebo.

141
Q

What does Topiramate (Topamax) do?

A

it is an approved anticonvulsant that prevents migraine, and weight loss

142
Q

What are the side effects of Topiramate?

A

mostly problems with memory, cognition and concentration, dizziness

143
Q

What is Qsymia?

A

Topiramata + phen combined

144
Q

What are the side effects of acomplia/Sanofi-aventis?

A

severe depression and suicidal thoughts by blocking Cannabinoid receptor (CB1), CB2 antagonist reverses leptin resistance in adipocytes and suppresses immune system; approved in the UK

145
Q

What does canabindoids regulate?

A

appetite, pain sensation, mood and memory, and plays a role in for successfulimplantationand early pregnancy maintenance

146
Q

What other drugs target Endocannabinoid system?

A

Contrave, Lorcaserin, Qnexa, and Pramlintide/Metreleptin

147
Q

How does Contrave/Orexigen work?

A

it is an inhibitor of norepi-dope uptake, and is a competitive antagonist of opioid receptors on POMC neurons to increase POMC activity. it is used to manage opioid and alcohol dependance, and has the potential to cause seizures

148
Q

What is Liraglutide?

A

FDA ever first approved injectable weight loss drug in 12/2012; stable peptide Used to counter insulin resistance in patience with type 2 diabetes by decreasing HbA1c, and because of this it helps for weight-loss; major side-effect is nausea and pancreatic cancer

149
Q

What is Amylin?

A

a small peptide hormone that is released by the β-cells of the pancreas along with insulin, after a meal. Absent in individuals with Type I diabetes.
slows gastric emptying, promotes satiety via hypothalamic receptors aids insulin by inhibiting glucagon

150
Q

How does Aspire Assist work?

A

Person withAspire Assisthas a tube surgically implanted through the abdomen into the stomach. 20-30 min After a meal, the food is drained and dumped into the toilet. The process takes about 10 minutes and the device can remove up to 30 percent of the calories consumed with a meal

151
Q

What is the phenotype of MC4-R Mutation?

A

Phenotype: hyperphagia starts at ~ 8 months; tendency toward being tall; hyperinsulinemia; increased bone mineral density
Some non-gentically obese patients have autoantibodies to MC4-R receptor leading to obesity

152
Q

What is the Methodological problem in discerning genome-wide associations?

A
  1. Power (we need to test genetics in a lot of people; = to increase sample size)
  2. Replication (test for association in independent ethnic groups)
  3. Biological validation for each associated variant; Evidence for pathophysiological role of the implicated gene
153
Q

What is the warm climate hypothesis?

A

Warm Climates, Slow Metabolism

OBESITY AND WEIGHTLOSS (3 decks)

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