ABSTRACT
In this study, it deals with 'Leptin' hormone, one of the most important endocrine hormones in the human body. Its working principle is on the physiology and the factors that it is effective on. It aims to show the physiology of leptin in an understandable and easily transferable way. It is one of the biggest reasons for me to choose this topic to show how great the role of this hormone is in our lives.
Internationally accepted articles, reviews and studies were based on and analyzed in this regard. Recent theories, concluded experiments and accepted transferred information are included. It was asked to convey this information to the reader in the cleanest way possible.
The importance of the working principle of leptin hormone for our vital continuities and its results are shown. In addition, information about its principles and exceptional circumstances was included.
Key Words: Leptin, Hormone, Physiology
TABLE OF CONTENTS
SYMBOLS, LIST OF ABBREVIATIONS
CNS Central Nervous System
PNS Peripheral Nervous System
It is the alpha symbol.
MSH Alpha Melanocyte Stimulating Hormone
CCK Cholecystokinin
NPY Neuropeptide
AgRP Agouti Related Peptide
Ob / ob Obese gene
Ra Rat
MAPK Mitogenic Interacting Protein Kinase
NTS Solitary Path Core
IL Interleukin
A CoA Acetyl Coenzyme A
Beta Symbol
DM Diabetes Mellitus
GH Growth Hormone
GIS Gastroinstestinal System
TRH Thyroid Relasing Hormone
IBF Insulin Growth Factor
PTP1B Protien Tyrosine Phosphatase 1 B
POMC Proopiomelanocortin
LepR Leptin Reseptr
Ng Nanogram
mL Mililitre
PEM Protein Energy Malnutrition
1. INTRODUCTION
Leptin, also called "satiety hormone", is a peptide hormone that regulates the appetite and fat stocks in the organism by creating a feeling of satiety. Leptin is secreted from fat (adipose) tissue, which is the body's largest endocrine organ. It acts on receptors in the hypothalamus. Adjusts the appetite to get energy homeostasis. Leptin, The importance of leptin was discovered in 1994 by Jeffrey M. Friedman and his colleagues at Rockefeller University in experiments on mice in a laboratory (Fve and Bastard, 2012).
Scientists started this discovery by realizing that mice with more leptin in their bodies were thinner and did not need to eat much. Leptin is mainly secreted by white adipose tissue and levels are positively correlated with the amount of body fat. Like many other hormones, leptin is secreted hazely and has a significant diurnal variation with higher levels in the evening and early morning. Circulating leptin levels reflect primarily the amount of energy stored in fat and secondarily acute changes in calorie intake. Leptin serves a critical evolutionary function by maintaining the relative constancy of adipose tissue mass, thus protecting individuals from the risks associated with being too underweight or overweight. Its concentration in the blood is generally proportional to body fat mass. It is more associated with testerone in men than in women. Hunger and chronic malnutrition cause a lower level of leptin in the blood. Leptin deficiency results in hunger, allowing the individual to eat to survive and also inhibit reproduction until their food and fat stores are sufficient to provide energy for pregnancy and breastfeeding. Therefore, leptin is important for the survival of the individual and for the survival of the species (Brennan & Mantzoros, 2006).
2. EFFECTS ON SYSTEMS
In this section, the effect of leptin on body systems, its importance and the situations in which it plays a role are given.
2.1 EFFECT ON THE CENTRAL NERVOUS SYSTEM
The nervous system in vertebrates consists of two main parts: the central nervous system (CNS) and the peripheral nervous system (PNS). The primary action of leptin is on the hypothalamus, which is part of the central nervous system. Leptin receptors are expressed not only in the hypothalamus but also in other brain regions, particularly the hippocampus. Thus, some leptin receptors in the brain are classified as central (hypothalamic) and some as peripheral (non-hypothalamic) (Halaas and Gajiwala, 1995).
As has been scientifically known so far, the general effects of leptin on the central nervous system are:
Leptin deficiency has been shown to alter brain proteins and neuronal functions of obese mice that can be restored with leptin injection. In humans, low circulating plasma leptin has been associated with cognitive changes associated with anorexia, depression and Alzheimer's disease. Studies in transgenic mouse models of Alzheimer's disease chronic administration of leptin improves brain pathology and cognitive has shown that it can improve performance (Leib et al., 2009).
In general, leptin is currently thought to enter the brain in the choroid plexus, where the intense expression of a leptin receptor molecule can act as a transport mechanism. Increased melatonin levels cause leptin regulation, however, melatonin is known to increase leptin levels in the presence of insulin and therefore cause a decrease in appetite during sleep. Partial sleep deprivation has also been associated with decreased leptin levels. Mice with type 1 diabetes treated with leptin or leptin plus insulin had better metabolic profiles compared to insulin alone: blood sugar was not fluctuated much; Cholesterol levels have been found to decrease (Pelleymounter and Cullen, 1995).
Leptin acts on receptors in the lateral hypothalamus to inhibit hunger and medial hypothalamus to stimulate satiety.
In the lateral hypothalamus, leptin inhibits hunger.
It has the ability to counteract the effects of neuropeptide Y, a strong hunger promoter secreted by cells in the gut and hypothalamus.
Resists the effects of anandamide, another potent hunger promoter that binds to the same receptors as THC.
Stimulates leptin satiety in the medial hypothalamus
Promotes hunger suppressing -MSH synthesis (Thomas, 2007).
Thus, a lesion in the lateral hypothalamus causes anorexia (due to the absence of hunger signals) and a lesion in the medial hypothalamus causes extreme hunger (due to the absence of satiety signals). This appetite inhibition is long-term, in contrast to the rapid inhibition of hunger by cholecystokinin (CCK) and slower suppression of hunger between meals mediated by PYY3-36. The absence of leptin (or its receptor) leads to uncontrolled hunger and ultimately obesity. Fasting or eating a very low-calorie diet lowers leptin levels. Leptin levels change more when food intake decreases than they increase (Augustyniak, Anderson, & Thomas, 2008).
Due to an acute change in energy balance, leptin dynamics may be associated with appetite and ultimately food intake rather than fat stores. Leptin binds to neuropeptide Y (NPY) neurons in the curved nucleus, reducing the activity of these neurons. Leptin signals the hypothalamus, which gives a feeling of fullness. What's more, leptin signals can make it easier for people to resist the lure of high-calorie foods. Leptin receptor activation inhibits neuropeptide Y and agouti-related peptide (AgRP) and activates -melanocyte stimulating hormone (-MSH). Npy neurons are an important element in the regulation of hunger; Selective destruction of npy neurons in mice makes them anorexic while small doses of npy injected into the brains of experimental animals stimulate feeding. Conversely, -MSH is an important mediator of satiety, and differences in the gene for the -MSH receptor have been linked to obesity in humans. Leptin interacts with six types of receptors Ob-Ra Ob-Rf or LepRa-LepRf encoded by a single gene, LEPR. Ob-Rb is the only receptor isoform capable of intracellular signaling via the jack-Stat and MAPK signal transduction pathways and is found in the hypothalamic nuclei. After leptin binds to the Ob-Rb receptor, it is phosphorylated and activates stat3 to the nucleus to affect changes in gene expression, one of the main effects is down-regulation of the expression of endocannabinoids responsible for increasing hunger. In response to leptin, receptor neurons have been shown to reshape themselves by changing the number and types of synapses firing at them (Doherty, Beccano-Kelly, Yan, Gunn-Moore, & Harvey, 2013).
