Changes

=== Increased desire to eat among the obese  ===

=== Increased desire to eat among the obese  ===

Charak correlated an increased desire to eat with increased ''agni'' in the morbidly obese. Recent evidence suggests that leptin and ghrelin had shown their influence on appetite. In this context, ghrelin is produced from the stomach, and leptin is produced by the adipose tissue of fat storage reserves in the body, which is responsible for short-term and long-term appetite control respectively in the body<ref>Hamann A, Matthaei S (1996). "Regulation of energy balance by leptin". Exp. Clin. Endocrinol. Diabetes104 (4): 293–300. doi:10.1055/s-0029-1211457. PMID 8886745. </ref>.  In the brain melanocortin pathway has drawn the attention of research scholars that this pathway has a specific role in stimulating appetite, which is located in the area of the lateral and ventromedial hypothalamus and arcuate nucleus. These areas are directly related to the feeding and satiety centers.<ref name=ref30>Rao CR, Sen PK, Flier JS (2012). Handbook of Statistics: Bioinformatics in Human Health and Heredity; Published by North Holland; 1 edition, Kindle Edition, 1 edition. </ref>  

Charak correlated an increased desire to eat with increased ''agni'' in the morbidly obese. Recent evidence suggests that leptin and ghrelin had shown their influence on appetite. In this context, ghrelin is produced from the stomach, and leptin is produced by the adipose tissue of fat storage reserves in the body, which is responsible for short-term and long-term appetite control respectively in the body<ref>Hamann A, Matthaei S (1996). "Regulation of energy balance by leptin". Exp. Clin. Endocrinol. Diabetes104 (4): 293–300. doi:10.1055/s-0029-1211457. PMID 8886745. </ref>.  In the brain melanocortin pathway has drawn the attention of research scholars that this pathway has a specific role in stimulating appetite, which is located in the area of the lateral and ventromedial hypothalamus and arcuate nucleus. These areas are directly related to the feeding and satiety centers.<ref name=ref30>,<ref>Rao CR, Sen PK, Flier JS (2012). Handbook of Statistics: Bioinformatics in Human Health and Heredity; Published by North Holland; 1 edition, Kindle Edition, 1 edition.</ref>  

There are two distinct groups of neurons in the arcuate nucleus viz- The first group contains neuropeptide Y (NPY) and agouti-related peptide (AgRP) and the second group contains Pro-opiomelanocortin (POMC) and cocaine and amphetamine regulated transcript (CART). The first group of neuron i.e. NPY/AgRP exerts stimulatory inputs to the LH while inhibitory inputs to the VMH, which stimulate feeding and inhibit satiety respectively. Both groups of arcuate nucleus neurons are the under the regulation of leptin, which inhibits the NPY/AgRP group of neurons and stimulating the POMC/CART group of neurons. Hence, the leptin deficiency or leptin resistance leads to develop overfeeding tendency, which is caused by some genetic and acquired forms of obesity.<ref name=ref30/>Rao CR, Sen PK, Flier JS (2012). Handbook of Statistics: Bioinformatics in Human Health and Heredity; Published by North Holland; 1 edition, Kindle Edition, 1 edition.  </ref>,  <ref>Raina GS (2011).Obesity being the major health burden needed to be chased: A systemic review. J Appl Pharm Sci. 2011;1:238–45.</ref> These findings suggest the genetic inputs in overweight and obesity, which is quite comparable to the Ayurvedic lexicons.[verse 4]

There are two distinct groups of neurons in the arcuate nucleus viz- The first group contains neuropeptide Y (NPY) and agouti-related peptide (AgRP) and the second group contains Pro-opiomelanocortin (POMC) and cocaine and amphetamine regulated transcript (CART). The first group of neuron i.e. NPY/AgRP exerts stimulatory inputs to the LH while inhibitory inputs to the VMH, which stimulate feeding and inhibit satiety respectively. Both groups of arcuate nucleus neurons are the under the regulation of leptin, which inhibits the NPY/AgRP group of neurons and stimulating the POMC/CART group of neurons. Hence, the leptin deficiency or leptin resistance leads to develop overfeeding tendency, which is caused by some genetic and acquired forms of obesity.<ref name=ref30/>Rao CR, Sen PK, Flier JS (2012). Handbook of Statistics: Bioinformatics in Human Health and Heredity; Published by North Holland; 1 edition, Kindle Edition, 1 edition.  </ref>,  <ref>Raina GS (2011).Obesity being the major health burden needed to be chased: A systemic review. J Appl Pharm Sci. 2011;1:238–45.</ref> These findings suggest the genetic inputs in overweight and obesity, which is quite comparable to the Ayurvedic lexicons.[verse 4]