Regulation of Food Intake (Lopez) Flashcards
1
Q
Where are neuronal centers located that control feeding/satiety?
A
hypothalamus:
- lateral nucleus (LH)
- ventromedial nucleus (VM)
- paraventricular nucleus (PV)
- dorsomedial nucleus (DM)
- arcuate nucleus (Arc)
2
Q
How is energy balance maintained within the body?
A
- crosstakl between neural and hormonal regulations
- hypothalamus receives many types of signals: neural signals from GI, chemical signals from nutrients in blood, signals from GI hormones, signals from adipose tissue, signals from cerebral cortex (sight, smell, taste)
3
Q
Where does most of the signaling integration take place regulating food intake/energy expenditure and what are the specific pathways?
A
arcuate nucleus
two pathways:
- part I: α-melanocortin (α-MSH) - α-MSH released by pro-opiomelanocortin (POMC) neurons, α-MSH binds to MCR-4 present in second-order neurons, anorexigenic pathway
- part II: neuropeptide Y (NPY) - hunger signals stim release of NPY, NPY binds to Y1R, agouti-related peptide (AGRP) also released (antagonist of MCR-4), orexigenic pathway
- both pathways antagonize each other: peptides that stim the α-MSH pathway inhibit the NPY system, AGRP is an antagonist of MCR-4
- some cases of obesity have been related to mutations in POMC and MCR-4 genes (pathway 1)
4
Q
genetic cause of obesity
- disease/disorder:
- sx: early-onset severe obesity, infertility (hypogonadotropic hypogonadism), hyperphagia, infections
- finding:
A
genetic cause of obesity
- disease/disorder: leptin or leptin receptor gene deficiency
- sx: early-onset severe obesity, infertility (hypogonadotropic hypogonadism), hyperphagia, infections
- finding: leptin
5
Q
genetic cause of obesity
- disease/disorder:
- sx: early-onset severe obesity, increased linear growth, hyperphagia, hyperinsulinemia, most common known genetic cause of obesity, homozygous worse than hetero
- finding:
A
genetic cause of obesity
- disease/disorder: melanocortin 4 receptor gene mutation
- sx: early-onset severe obesity, increased linear growth, hyperphagia, hyperinsulinemia, most common known genetic cause of obesity, homozygous worse than hetero
- finding: MC4R mutation
6
Q
genetic cause of obesity
- disease/disorder:
- sx: neonatal hypotonia, slow infant growth, small hands/feet, mental retardation, hypogonadism, hyperphagia leading to severe obesity, paradoxically elevated ghrelin
- finding:
A
genetic cause of obesity
- disease/disorder: Prader-Willi syndrome
- sx: neonatal hypotonia, slow infant growth, small hands/feet, mental retardation, hypogonadism, hyperphagia leading to severe obesity, paradoxically elevated ghrelin
- finding: partial deletion of chromosome 15 or loss of paternally expressed genes
7
Q
genetic cause of obesity
- disease/disorder:
- sx: obesity, red hair, adrenal insufficiency due to ACTH deficiency, hyperproinsulinemia, hyperphagia, pale skin, cholestatic jaundice
- finding:
A
genetic cause of obesity
- disease/disorder: proopimelanocortin (POMC) deficiency
- sx: obesity, red hair, adrenal insufficiency due to ACTH deficiency, hyperproinsulinemia, hyperphagia, pale skin, cholestatic jaundice
- finding: loss of function mutations of POMC gene
8
Q
How could the vagus nerve be used in feeding behavior therapies?
A
- several peptides that stim satiety/decrease feeding activate receptors on vagal afferents
- vagal > NTS > hypothalamus circuit prod responses related to feeding behavior/metabolism
- if vagal activity is blocked, the amnt of material in stomach no longer influences meal size
9
Q
What is the role of vagal > NTS > hypothalamus circuit in feeding behaviors?
A
- NTS: crucial in interpretation and relaying of peripheral signals
- vagal signaling to NTS is integrated w/ info received by hypothalamus to prod appropriate feeding behavior/metabolic responses
- hindbrain is able to regulate food intake in response to peripheral signals even in absence of higher centers’ input
10
Q
- hunger center within the hypothalamus
- neurons project throughout brain and release the orexigenic peptides melanin-concentrating hormone (MCH) or orexins A and B
A
lateral hypothalamic area (LHA)
11
Q
satiety center within the hypothalamus
A
ventromedial hypothalamic nucleus (VMN)
12
Q
nucleus within the hypothalamus that contains neurons that project to both cerebral cortex and areas of the brainstem
A
paraventricular nucleus (PVN)
13
Q
Hormones released for the ___ ______, ________, and _______ _______ regulate feeding behaviors.
A
Hormones released for the GI tract, pancreas, and adipose tissue regulate feeding behaviors.
14
Q
- secreted in the stomach by endocrine cells
- binds to growth hormone secretagogue receptors (GHSR)
- stimulates neurons that release NPY
- actions, increase appetite, gastric motility, gastric acid secretion, adipogenesis, decrease insulin secretion (although evidence for both inc/dec insulin)
- appears to initiate the feeding response
A
ghrelin
15
Q
- hormone that binds to receptors in POMC (stimulates) and NPY (inhibits) systems
- actions: decrease appetite, increase metabolism
- in patients w/ type DM, there is an increase in food intake a/w decrease in this hormone
A
insulin
16
Q
- hormone released by I cells in duodenum
- elicits satiety: acts on vagal > NTS > hypothalamus circuit to decrease ghrelin; and decreases gastric emptying by increasing gastric distention
A
CCK
17
Q
- hormone released by L cells of the ileum and colon following a meal
- binds to Y2R in the hypothalamus: inhibits NPY neurons, releases inhibition of POMC neurons
A
PYY
18
Q
- hormone secreted by cells in adipose tissue
- binds to receptors in POMC (stimulates) and NPY (inhibits) systems
- appetite-supressing hormone: decreases appetite and ghrelin release, increases metabolism
- in obese children w/ congenital deficiency of this hormone, subcu administration of recombinant hormone reduces fat mass, hyperinsulinemia, and hyperlipidemia
- obesity in adults is often a/w high hormone levels and failure to respond to exogenous hormone (hormone resistance)
A
leptin
19
Q
Hormone regulation summary:
A
20
Q
summary of the integration of signals regulating food intake and energy expenditure:
A
21
Q
What is the differences between adipose signaling vs gut signaling?
A
- adipose signals (leptin) are involved in long-term regulation of energy
- gut peptides (PYY from intestines, ghrelin from stomach) modulate food intake on a meal by meal basis
27
Q
- condition characterized by self-starvation and excessive weight loss
- patients become severely malnourished and significantly emaciated, leading to endocrinological and cardiological dysfunctions, and abnormalities within digestive, skeletal, and repro systems
A
anorexia nervosa
28
Q
What biological factors related to gut-brain axis support restricted eating in patients w/ anorexia?
A
- polymorphisms present in genes involved in eating attitudes, regulation of eating behavior, motivation, and reward mechanisms (e.g. AgRP)
- basal and pulsatile secretion of leptin is reduced in a/w reduction in fat mass
- ghrelin resistance appears to be a conducive factor to a restrictive diet
- elevated levels of PYY: might contribute to decreased nutrient intake and disordered eating psychopathology
