Hunger Responses: How Brain Could Function To Increase The Chance Of Survival During Starvation

Food is a basic necessity of life; it makes people live and do their routine effectively. People cannot perform well in their everyday tasks if they are hungry. Hunger is a longing or crucial need for food or a particular nutrient. A new study about hunger responses was recently released.

According to Nagoya University, the human body reacts to starving situations such as famine to raise the likelihood of survival. It decreases energy output by impeding heat formation and induces eating behaviors. These hunger responses are stimulated through the sense of hunger in the stomach.

Neuropeptide Y (NPY) signals controls the hunger responses. The neuron in the hypothalamus releases these signals. NPY signaling in the hypothalamus that triggers the hunger responses is still strange.

Sympathetic motor neurons found in the medulla oblongata are accountable for heat formation with the help of brown adipose tissue (BAT). The researchers from Nagoya University now experimented whether these neurons react to similar hypothalamic NPY signals that command hunger responses.

They injected NPY into the hypothalamus of rats and assessed the result on heat production. Blocking inhibitory GABAergic receptors and stimulating excitatory glutamatergic receptors are located in the sympathetic motor neurons. They give rise to heat production under normal situation.

However, stimulating glutamatergic receptors did not generate heat while inhibiting GABAergic receptors did following NPY injection. The research was recently circulated in Cell Metabolism.

"This indicated that hypothalamic NPY signals prevent BAT thermogenesis by using inhibitory GABAergic inputs to sympathetic motor neurons," study lead author Yoshiko Nakamura says. Retrograde and anterograde tracing with fluorescent dyes shows which brain part yielded the inhibitory GABAergic inputs to heat-producing motor neurons.

The tracing tests displayed that sympathetic motor neurons are clearly innervated by GABAergic inputs located in reticular nuclei of the medulla oblongata, co-author Kazuhiro Nakamura interpreted. Particular stimulation of these GABAergic reticular neurons suppress BAT thermogenesis he added.

The researchers conducted additional investigation and found out that GABAergic inputs are participating in hypothalamic NPY-mediated inhibition of heat production in BAT. This hunger response circuit apparently interprets why anorexic people experience hypothermia.

Triggering these medullary reticular neurons motivated rats to start chewing and feeding. This outcome was the same with NPY injection into the hypothalamus. It proposes that hypothalamic NPY signaling drives reticular neurons in the medulla oblongata to induce feeding and chewing throughout the hunger response.

As per Science Daily, obesity is one of the main causes of dangers to the health of U.S. citizens. It induces the progression of many serious medical problems such as diabetes, heart disease and some kinds of cancer. However, obesity is scarcely included in a medical training, according to the latest research of Northwestern Medicine.

Obesity could arise from an abnormal stimulation of the mentioned neurons under non-starved conditions. Therefore, a wide knowledge to those mechanisms might lead in the advancement of more competent solutions for obesity.