Obesity Flashcards
chronic condition defined as an excess of body fat or adipose tissue that causes disease.
Obesity
A normal BMI
18.5 and 24.9 kg/m2
overweight
BMI between 25 and 29.9 kg/m2
class I obesity
BMI of 30 to 34.9 kg/m2
class II obesity
BMI of 35 to 39.9 kg/m2
class III obesity
BMI greater than 40 kg/m2
Complications of obesity
type 2
diabetes, stroke, heart disease, NAFLD, and several types of
cancer, all of which are considered obesity-related causes of
preventable death globally
Dietary Factors
These studies favor a high-protein, low-carbohydrate diet for
avoidance of excess weight gain.
high-protein diets
may be favorable are increased satiety, increased thermic effect
of food, and improved body composition.
Medication-Induced Weight Gain
antipsychotics (e.g., olanzapine, clonazapine),
antidepressants (e.g., the SSRI, paroxetine), anti-epileptics (e.g., valproate, gabapentin), insulin and insulin secretagogues (e.g., thiazolidinediones),
glucocorticoids,
progestational hormones and implants,
oral contraceptives,
beta-blockers
Smoking
first, smoking is thermogenic—that is, the metabolic rate
during the act of smoking is higher than when the subject is not
smoking;
second, smoking reduces hunger and changes taste perception so smokers tend to eat less.
Genetics
The melanocortin-4 receptor (MC4R) gene, leptin gene, pro-opiomelanocortin (POMC) gene, and agouti gene all have significant effects on body fat and fat stores.
Obesity, mental retardation, brachymetaphalangism, short stature
Missense, frameshift, nonsense, splice-site, deletions, insertions in GNAS1/GNAS. Autosomal dominant
Albright hereditary osteodystrophy/ pseudohypoparathyroidism type Ia
Childhood obesity, insulin resistance and type 2 diabetes mellitus, blindness, hearing impairment
Frameshift, nonsense, missense in ALMS1. Autosomal recessive
Alström syndrome
Obesity, retinitis pigmentosa, renal malformation, polydactyly, mental retardation, hypogonadism
Missense, nonsense, splice-site and frame-shift mutations in BBS1, BBS2. Autosomal recessive
Bardet-Biedl syndrome/Laurence- Moon-Bardet-Biedl syndrome
Obesity, umbilical hernia, soft tissue syndactyly, congenital heart disease, mental retardation, hypogenitalism
Truncating, missense, nonsense mutations of RAB23. Autosomal recessive
Carpenter syndrome/ acrocephalopolysyndactyly type II
Obesity and hyperphagia, failure to thrive, hypotonia, genital hypoplasia, mental retardation, small hands and feet
Deletions, mutations, loss of paternal allele MKRN3/ ZNF127/MAGEL2. Autosomal dominant, x-linked
Prader-Willi syndrome/Prader- Labhart-Willi
Leptin
Absence of leptin or an ineffective leptin receptor is associated with severe obesity
Leptin has the dual effect of reducing food
intake and increasing energy expenditure, both of which favor
loss of body fat.
Treatment of leptin-deficient children with
leptin decreased their body weight and hunger, indicating
the importance of leptin in normal subjects.
PATHOPHYSIOLOGY OF OBESITY
One body of neurons expresses the orexigenic peptides neuropeptide Y and agouti-related peptide, each of which function to increase food intake and reduce energy expenditure.
express POMC, and cocaine- and amphetamine-regulated transcript, which are anorexigenic peptides that lead to a reduction in appetite and increase in energy expenditure by activation of downstream pathways, such as activation of MC4R in the para- ventricular nucleus of the hypothalamus.
Damage to POMC neurons
Damage to POMC neurons and concomitant inflammation has been associated with diet-induced obesity and resistance to weight-regulating hormones including leptin and insulin
reduce food intake
Intestinal peptides, including glucagon-like peptide (GLP),
CCK, pancreatic polypeptide, and polypeptide YY
stimulates food intake
ghrelin, a small peptide produced in the stomach
an enzyme that is activated or inhibited in relation to the ratio
of adenosine monophosphate to adenosine triphosphate and is
thought to be the underlying central point in the control system of food intake
Oxidation of fatty
acids modulates activity of 5′-adenosine monophosphate kinase
Waist circumference
Waist circumference should be measured with the proper technique at the level directly above the iliac crests, especially in patients with a BMI greater than 25 to 35 kg/m2 who will require further risk stratification