BIOL 2420 Lecture Notes - Lecture 1: Knockout Mouse, Adipose Tissue, Adipocyte
26 Apr 2018
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Unit 10 – Lecture 1
Appetite and Satiety
- Control of food intake = complex process
- Digestive system does not regulate energy intake
o Need behavioural mechanisms such as hunger and satiety to tell us when and how much
to eat
o Psychological and social aspects of eating – parets ho say lea your plate –
complicate the physiological control of food intake
o Still do not fully understand what governs when, what, and how much we eat
- Current model for behavioural regulation of food intake is based on two hypothalamic centers
o Feeding center – tonically active
o Satiety center – stops food intake by inhibiting the feeding center
- Output signals from these centers cause changes in eating behaviour and create sensations of
hunger and fullness
o Destroyed feeding centers = cessation of eating
o Destroyed satiety = animals overeat and become obese
- Study using transgenic and knockout mice
o Hypothalamic centers form a complicated neural network whose neurons secrete a
variety of chemical messengers
o Control of food intake is complex
▪ Higher brain centers, including the cerebral cortex and limbic system, provide
input to the hypothalamus
o Many different chemical signals influence food intake and satiety
▪ Including neuropeptides – brain-gut hormones secreted by the GI tract, and
chemical signals called adipocytokines, which are secreted by adipose tissue
- Two classic theories for regulation of food intake
o Glucostatic theory
▪ Glucose metabolism by hypothalamic centers regulates food intake
▪ Blood [glucose] decrease = satiety center suppressed, feeding center is
dominant
▪ Glucose metabolism increases, satiety center inhibits feeding center
o Lipostatic theory of energy balance
▪ “igal fro the ody’s fat stores to the rai odulates eatig ehaiour =
body maintains a particular weight
▪ Fat stores are increased = eating decreases
▪ During times of starvation = eating increases
▪ Obesity results from disruption of this pathway
- Discovery of leptin
o Provided evidence for Lipostatic theory
o Leptin – protein hormone synthesized in adipocytes
▪ Acts as a negative-feedback signal between adipose tissue and the brain
▪ Fat stores increase, adipose cells secrete more leptin, and food intake decreases
▪ Synthesized in adipocytes under control of obese (ob) gene
• Mice lacking ob gene become obese
• Mice with defective leptin receptors have the same effect
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Control of food intake = complex process. Current model for behavioural regulation of food intake is based on two hypothalamic centers: feeding center tonically active, satiety center stops food intake by inhibiting the feeding center. Output signals from these centers cause changes in eating behaviour and create sensations of hunger and fullness: destroyed feeding centers = cessation of eating, destroyed satiety = animals overeat and become obese. Including neuropeptides brain-gut hormones secreted by the gi tract, and chemical signals called adipocytokines, which are secreted by adipose tissue. Leptin is only part of the story in humans. Key signal neuropeptide y (npy: brain neurotransmitter that seems to be the stimulus for food intake, normal weight animals leptin inhibits npy in a negative feedback pathway. Other neuropeptides, hormones, and adipocytokines also influence npy secretion, leptin release by adipocytes, and the hypothalamic centers controlling food intake.
