Final answer:
The hypothalamus integrates hunger and satiety signals to regulate feeding, with the genetic deletion of the ob gene resulting in unregulated feeding due to lack of leptin.
Step-by-step explanation:
Regulation of Feeding by the Hypothalamus
The hypothalamus plays a central role in the regulation of feeding by coordinating various hunger and satiety signals. It consists of a collection of nuclei involved in regulating homeostasis, including energy balance through feeding behavior. These nuclei integrate signals from a wide array of neurons and peptides associated with energy homeostasis.
Consequences of Genetic Deletion of the ob Gene
The ob gene encodes for leptin, a hormone crucial for long-term regulation of energy balance. Its deletion leads to the absence of leptin, resulting in unregulated feeding and obesity, as the hypothalamus lacks the signal to suppress hunger.
Hypothalamic Response to Leptin Levels
With elevated leptin levels, anorexigenic neurons, including those producing MSH (melanocyte-stimulating hormone) and CART (cocaine- and amphetamine-regulated transcript), are activated to suppress appetite. In contrast, decreased leptin levels activate orexigenic neurons, such as those producing NPY (neuropeptide Y) and AgRP (agouti-related protein), which stimulate appetite.
Role of MCH and Orexin in the Lateral Hypothalamus
MCH (melanin-concentrating hormone) and orexin, produced by neurons in the lateral hypothalamus, also regulate feeding. MCH generally promotes feeding, whereas orexin increases arousal and may stimulate feeding under certain conditions. Both play differing roles in the complex circuitry controlling energy balance.