HBS202 Advanced Physiology: Leptin, Obesity, and Appetite Control

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This presentation delves into the role of leptin, a peptide hormone produced by white adipose tissue, in regulating appetite and satiety. It discusses leptin's production, regulation of release by factors like insulin, receptor locations in the CNS (brain stem, hypothalamus, reward centers), and activated cell signaling pathways such as PI3K. The presentation elucidates how leptin influences food intake by acting on the brain to control appetite and energy expenditure, highlighting its long-term effects and its involvement in obesity. It explains how leptin signals satiety to the hypothalamus, modulates energy expenditure, and affects carbohydrate metabolism, while also noting the phenomenon of leptin resistance in obesity. References to relevant research articles are included.
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ADVANCE SYSTEM
PHSYIOLOGY
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Table of content
Where is your chosen peptide produced?
What regulates its release?
Where are the receptors for your chosen peptide located and which cell signaling pathway
is activated following receptor activation (keep this simple).
How does your chosen peptide regulate food intake?
Role of leptin in obesity?
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Where is your chosen peptide produced?
Leptin is a 16-kDa peptide hormone which is produced from white adipose tissues from an individual's
body
It helps in balancing between energy intake and energy utilization by the body.
This hormone helps in binding to hypothalamic receptors and modulating diet control centres in the
brain of an individual.
Leptin is encoded by the obese gene.
It include metabolism, endocrine regulation and immune function.
The amount of leptin hormone within blood stream is directly proportional to the amount of adipose
tissue.
The most known as action of the action is known as ARC nuclei, ARC nucleus plays a significant role in
activation of such areas and leads changes including thyroid, gonad and others.
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What regulates its release?
Leptin is a hormone which is generally secreted from the fat cells which aid to regulates the
weight of the body. The insulin is an essential factor in the stimulation of the secretion of
leptin.
The insulin hormones can regulates the long term secretion of the leptin of the adipose cells
by the mechanisms such as transcriptional or post-transcriptional. The leptin peptide
generally circulates in the blood and can acts on the human brain so as to regulates the
intake of the food products as well as the expenditure of the energy.
Generally when the fat mass falls, the level of the plasma leptin will also falls. This
generally enhances the appetite as well as can suppress the expenditure of the energy until
when the fat mass is being stored.
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Leptin receptor and their signaling pathway
Leptin receptors are found in the each of the major components of the CNS in the feeding circuitry the
brain steam, hypothalamus and distributed reward centers . Through this receptor, leptin exerts
influences on the singling and integration within these circuits to alter feeding behaviors. Leptin and
insulin signaling pathways converge on the phosphatidylinositol 3 kinase PI3K. Activation of the PI3K
by either leptin lead to the phosphorylation of the Forehead box 01 through the Act, which can also
activate the mammalian target of the rapamycin.
Leptin receptors also called as the obesity receptors, molecules that receives and transmit through
signals from the leptin and a hormonal released from the fact cells, involved in the primarily in the
regulation of the metabolism. This also several role in the bone metabolism and immunity along with
the reproductive functions. This protein receptors activate the multiple signaling pathway.
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How does your chosen peptide regulate food
intake?
There is high impact on the Leptin which can exerts immediate effect through acting on brain to regulate
individual appetite.
This is the one when individual body is functioning properly then there is production of excess fat cells
which are effective and allow to produce leptin that is effective to trigger the hypothalamus which is
effective to lower the appetite level and allow human body to get dip into stored fat to feed itself. Leptin
doesn’t have direct impact on the food intake, instead of this, they act to alter the food intake along with
control the energy expenditure for long term.
Leptin contribute in the development and maintenance of obesity. Through using the property to increase
the weight loss allow the regulation of food intake and have high influence on the energy level. There is
high impact of Leptin which is more profound effect when there is loss in the body weight and hormone
level falls.
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Leptin role in obesity
As per this, the major role of leptin in the body weight regulation is by the way to signal
satiety to the aspect of hypothalamus and thus they can reduce the dietary intake.
The storage which is associated with the fats while they are modulating energy expenditure
and then they convert the metabolism which is related with the carbohydrate which help to
prevent the upcoming weight gain.
Because, usually leptin reduce and the food intake, the existence which show the
enhancement leptin level with the obesity or the overweight which is widely determined as
the evidence of leptin resistance. As per this, the obesity is being promoted with the
multiple cellular process that is attenuated leptin signalling that refers as the cellular leptin
resistance and they are complete amplified.
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References
Gambineri et. al., 2019. Female infertility: which role for obesity? International journal of obesity
supplements, 9(1), pp.65-72.
Monteiro et. al., 2019. Leptin in the regulation of the immunometabolism of adipose tissue‐macrophages. Journal
of leukocyte biology, 106(3), pp.703-716.
Packer et. al., 2018. Leptin-aldosterone-neprilysin axis: identification of its distinctive role in the pathogenesis of
the three phenotypes of heart failure in people with obesity. Circulation, 137(15), pp.1614-1631.
Song et. al., 2018. Leptin induces SIRT1 expression through activation of NF-E2-related factor 2: Implications for
obesity-associated colon carcinogenesis. Biochemical pharmacology, 153, pp.282-291.
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