Unit 3 Pathophysiology - Chapter 23 Obesity and Disorders of Nutrition Flashcards
Adipose tissue
- insulation
- tissue support
- energy reserve - storing triglycerides and glycerol (from glucose) => released at later time for metabolic use
Is adipose considered an organ?
Yes, an endocrine organ that secrete hormones called adipokines (w/ paracine, autocrine, and endocrine actions => metabolic and immune responses)
* can control inflammatory response, insulin sensitivity
White adipose tissue (WAT)
- stromal structure containing macrophages, mast cells, neutrophils, fibroblasts, endothelial cells, blood vessels, nerves, and precursor adipocytes
- largest fat deposit; located in visceral (central, surrounding areas of organs) and subcutaneous (peripheral) sites, including muscle + bone marrow
- STORES fat as a single lipid droplet (lipid rich organelle that regulate storage and hydrolysis of lipids) or vacuole
- With positive energy balance, visceral fat increasing via adipocyte hypertrophy (increase in size) while subcuteanous fat increasing via adipogenesis (increase in number of adipocyte cells)
Estrogen and fat deposit bx?
Estrogen enhances deposition of subcutaneous fat compared to visceral fat
Brown adipose tissue (BAT)
- Multiple lipid droplets
- rich in mitochondria containing iron (which gives BAT the brown color)
- Exposure to cold OR sympathetic activation and release of catecholamines, and activation of T3 generate heat via activation of UCP1 (uncoupling protein 1 - found in mitochondrial inner membrane of BAT helps facilitate process of non-shivering thermogenesis in mammals) and free fatty acid oxidation
- thyroid hormone triiodothyronine (T3) activates thermogenesis by uncoupling electron transport from ATP synthesis in brown adipose tissue (BAT) mitochondria.
- Present upon birth very little
BAT vs WAT amount
Neonates and adults have BAT, but not as much as WAT (neonates)
How does bAT (beige) emerge?
Starts from within WAT d/t exposure to cold, exercise, and synthetic ligands of PPARy (gamma) [regulator of lipid and glucose metabolism, such as the synthetic ligand glitazone, improve insulin and glucose parameters while increasing whole body insulin sensitivity]
* Known as “beiging” of WAT
BAT and bAT can?
Protect against obesity and metabolic syndrome
Inside muscles,myokines irisin and fibroblast growth factor 21 can
- irisin (produced in response to exercise) w/ protective factors gainst central and peripheral nervous system
- factor 21 - energy homeostasis and adaptation to starvation and low temp
- both can activate BAT and bAT for thermogenesis and protect against obesity
Brown adipose tissue
Bone marrow adipose
- releases adipokine
- and it communicates with osteoclasts to maintain bone structure
How is obesity defined?
- BMI >30 kg/m2 in adults
Hypothalamus
- this center (regulates food intake + energy expenditure) including some other brain center
- specifcally in the arcuate nucleus (w/ 2 opposing neurons): manage the above fx’s
- orexigenic neurons => promote appetite, stimulate eating, decrease metabolism
- anorexigenic neurons => suppress appetite/eating, increase metoblism
Brain centers r/t reward, pleasure, and memory
can override hypothalamic food control + satiety
* causing increased consumption of highly palatable foods
* l/t increased fat stores
Relationship between leptin levels and obesity
Both increase together (leptin resistance - hormone maintains your normal weight by regulating appetite)
cause:
* overeating
* insulin resistance
* hyperinsulinemia (more insulin in blood, d/t resistance)
* hyperlipidemia
* stimulate adipocyte endothelial cells
* macrophages induce more obesity
RBP4
- increased w/ visceral diposity while promoting insulin resistance and hepatic steatosis
- crucial in Vitamin A interaction => teeth, skeletal/soft tissue, mucus membrane, skin + pigments in eye retina
Adiponectin levels
- decrease w/ obesity l/t insulin resistance, inflammation, and hyperlipidemia
- adipokine (cytokine) secreted by adipocytes => regulates glucose levels, lipid metabolism, and insulin sensitivity
Endocannabinoids
- Increased with obesity
- promotes food intake, lipogenesis, stops energy expenditure
Angiotensin I and II
increase w/ obesity
* promoting vasoconstriction
* inflammation
* lipogenesis, insulin resistance
* oxidative stress
Ghrelin
- increases with obesity and stimulates food intake, GH, & lipogenesis
- other protective factors it has: satiety, vasodilatory, cardioprotective, and antiproliferative effects (unknown in obesity control)
Glucagon-like peptide 1
- promotes insulin secretion
- delays gastric emptying
- suppresses appetite
- increases energy expenditures
- DECREASED w/ obesity onset
- this, peptide YY, and Adiponectin levels decrease
Peptide YY
- inhibits gastric motility, decreaes appetite, and decreased with obesity
What state does obesity cause?
state of chronic low grade inflammation caused by
* adipocyte macrophages
* neutrophils
* lymphocytes
What are 3 general causes contribute to obesity?
- chronic inflammation
- alterations in adipokine action
- accelerated lipolysis r/t excessive fat
anorexia nervosa
Anorexia nervosa is a psychiatric disease in which patients restrict their food intake relative to their energy requirements through eating less, exercising more, and/or purging food through laxatives and vomiting. Despite being severely underweight, they do not recognize it and have distorted body images
- Poor nutritional status
- Dehydration
- Being very thin
- Stomach pain or bloating
- Constipation
- Lethargy or fatigue
- Unable to handle cold temperatures
- Fine, downy body hair (called lanugo)
- Dry or yellowish skin
- Thinning hair
- Brittle nails
bulimia nervosa
Bulimia is an eating disorder. It is characterized by uncontrolled episodes of overeating, called bingeing. This is followed by purging with methods such as vomiting or misuse of laxatives. Bingeing is eating much larger amounts of food than you would normally eat in a short period of time, usually less than 2 hours. You may feel like you can’t stop or control these episodes of binge eating.
The binge-purge cycles can happen from many times a day to several times a week.
Often, people with bulimia keep a normal or above normal body weight. This lets them hide their problem for years. Many people with bulimia don’t seek help until they reach the ages of 30 or 50. By this time, their eating behavior is deeply ingrained and harder to change.
There are 2 ways people with bulimia restrict calories:
- Purging type. The person engages in self-induced vomiting or misuse of laxatives, diuretics, or enemas, or other medicines that clear the intestines.
- Nonpurging type. The person uses other behaviors, such as fasting or excessive exercise, rather than purging behaviors.
- Swollen salivary glands
- Cut or callused knuckles from self-induced vomiting
- Tooth enamel erosion from contact with stomach acid during self-induced vomiting
- Gastrointestinal problems such as stomach cramps, acid reflux and constipation
Potential health complications of bulimia include:
- Loss of menstrual period (amenorrhea) and infertility in girls
- Severe dehydration, which can lead to seizures or kidney failure
- Electrolyte imbalance, which can lead to irregular heartbeat, heart failure, stroke or seizures
- Stomach damage
- Esophagus damage
- Insulin resistance, which can cause Type 2 diabetes
binge eating disorder
Binge-eating disorder is a serious eating disorder in which you frequently consume unusually large amounts of food and feel unable to stop eating.
Almost everyone overeats on occasion, such as having seconds or thirds of a holiday meal. But for some people, excessive overeating that feels out of control and becomes a regular occurrence crosses the line to binge-eating disorder.
When you have binge-eating disorder, you may be embarrassed about overeating and vow to stop. But you feel such a compulsion that you can’t resist the urges and continue binge eating. If you have binge-eating disorder, treatment can help.
How does body repsond to short-term starvation?
By protecting protein mass:
* using glycogenolysis (glycogen => glucose)
* gluconeogenesis (glucose formed frrom glycerol, lactate, pyruvate, and glucogenic amino acids)
Long-term starvation mechanisms
- initial decreased dependence on gluconeogenesis and increased use of ketone bodies as a energy source
- FOLLOWED by lipolysis in adipose tissue
- absence of adequate nutrition => proteolysis d/t eletrolyte imabalance and loss of renal, pulmonary, and cardiac function
Aging and anorexia
less appetite or food intake in OA; l/t undernutrition and result in decline in fx and increased ris kfor morbidity and mortality
