describe both the hormonal and neural control of eating.

Hormonal and Neural Control of Eating
Feeding is largely impacted by peptides and steroids in the body. They influence appetite by impacting the autonomic nervous system, the hypothalamus and brainstem (Murray, Tulloch, Gold & Avena, 2014). They are excreted from the gastrointestinal tract, the fat cells and the pancreas. A good example is Leptin. Leptins are dopaminergic receptors located in the ventral tegmental area. They serve to limit appetite levels reducing weight (Murray et al., 2014). Gherin, also referred to as orexigenic hormone is also associated with feeding. It is associated with high appetite levels and feeding. Gherin administration has been linked with high dopamine concentration and hyperactivity. It raises acetyl choline in the VTA hence incentivizing the intake food.
Increasing the Leptin levels will, as a result, reduce body weight and appetite. I would rather have the ob/ob genetic mutation rather than the db/db since it is reversible. Linking an ob/ob mouse with a normal mouse would result in weight reduction for the obese rat. Linking a db/db mouse would shrink the normal mouse and consequently result in weight reduction for the ob/ob mouse. Giving the animal ghrelin would feel hungrier and gain appetite levels hence the animal, as a result, take in more food and increase its fat storage. Upon lesion of the ventromedial hypothalamus, the animals would eat excessively and become obese. Upon lesion the lateral hypothalamus of an animal the animals would become thinner as a result of becoming anorectic (Murray et al.

, 2014).
I would rather have the lateral hypothalamus dysregulation as the ventromedial has far much wider effects. Ventromedial hypothalamus impacts cannabinoid receptors which are associated with rewarding and dopamine excretion from the brain (Murray et al., 2014). Impacting dopamine levels serves to impact sexual activity. In rat experiments, VMH served to increase plasma insulin rates. This, as a result, escalates Leptin production initiating obesity. Lateral hypothalamus, on the other hand, initiates motility as well as eating disorders. It impacts the appetite-regulators, that is, Leptin and Gherin reducing appetite levels (Murray et al., 2014).
Reference
Murray, S., Tulloch, A., Gold, M. S., & Avena, N. M. (2014). Hormonal and neural mechanisms of food reward, eating behaviour and obesity. Nature Reviews Endocrinology, 10(9), 540.