Summary: A new study reveals that a high-fat diet alone does not appear to be responsible for changes in brain neurons that regulate appetite and energy balance. The researchers found no immediate effect on neurons in the hypothalamus of mice fed a high-fat, low-carbohydrate diet, suggesting that other nutrients like sugar may play a more important role in changes in brain function. This suggests that it may be possible.
This study questions previous assumptions that fat alone is responsible for disrupting energy homeostasis and increasing the risk of metabolic disease. Future research will investigate how different macronutrients affect neurons in the brain and the regulation of appetite.
Important facts:
High-fat diet alone did not affect AgRP neurons in the hypothalamus. Other nutrients, such as sugar, can have even more profound effects on brain function. Both male and female mice showed no decrease in neuronal connectivity even after 48 hours of chow.
Source: DZD
High-fat diets can promote overweight and increase the risk of metabolic diseases such as diabetes. In the mouse brain, this causes measurable changes in the hypothalamic region.
However, as a research team from the German Institute for Human Nutrition Potsdam-Lebrücke (DIfE) and the German Diabetes Research Center (DZD) reported in the journal Scientific Reports, fat is not the only culprit. Apparently not.
The connections between neurons in the brain are constantly changing. Diet has a big influence on this. It is now known that high-fat diets can cause changes in the hypothalamus, disrupting energy homeostasis and increasing the risk of metabolic diseases.
Food intake is primarily controlled in the brain by two types of neurons: AgRP (agouti-related peptide) neurons and POMC (proopiomelanocortin) neurons. Both are located primarily in the hypothalamus, more precisely in the central region of the hypothalamus, the paraventricular nucleus, and have opposite effects. POMC neurons suppress food intake, whereas AgRP neurons promote food intake.
Fat, or rather sugar?
Previous studies have shown that AgRP neuron activity in the paraventricular nucleus is reduced in mice fed a high-fat diet. This was mainly due to the high fat content of the feed given to the animals.
However, the mouse diets studied also contained other nutrients, such as sugar. Therefore, it is not possible to say with certainty which macronutrient is responsible for the neuronal changes.
DIfE and DZD researchers investigated whether fat is primarily responsible for causing changes in the brain. The researchers fed male and female mice a high-fat, low-sugar diet for 48 hours.
It was important for the researchers to study both male and female mice, as previous studies have often used only males. As a result, it was unclear whether men and women responded differently to high-fat diets.
Other nutrients that are more important
Examination of the animal’s brain yielded unexpected results. No effect of high-fat diet was observed. AgRP neuron connectivity was not reduced in either female or male mice.
This suggests that dietary fat (alone) is not responsible for the previously observed hypothalamic changes. The researchers suspect that other macronutrients, such as sugar, may have an even more profound effect on AgRP neurons.
They now hope to conduct further studies to investigate the role of individual macronutrients on neuroanatomical and functional changes in the brain.
About this appetite and neuroscience research news
Author: Birgit Niessing
Source: DZD
Contact: Birgit Niesing – DZD
Image: Image credited to Neuroscience News
Original research: Open access.
Selma Yagoub et al. “Acute elevation of dietary fat is not sufficient to reduce AgRP projections in the paraventricular nucleus of the hypothalamus in mice.” scientific report
abstract
Acute elevation of dietary fat alone is not sufficient to reduce AgRP projections in the paraventricular nucleus of the hypothalamus in mice
In the brain, connections between neurons are constantly changing in response to environmental stimuli. The main environmental regulator of neural activity is diet, and previous studies have highlighted changes in hypothalamic connectivity in response to diets high in dietary fat or increased sucrose.
We sought to determine whether changes in hypothalamic neural connectivity are primarily caused by increases in dietary fat alone. Analyzes were performed on both male and female animals.
We measured agouti-related peptide (AgRP) neuropeptide and synaptophysin markers in the paraventricular hypothalamic nucleus (PVH) in response to a 48-h acute high-fat dietary challenge.
Using two image analysis methods described in previous studies, we did not confirm the effect of high-fat diet on AgRP neuron projections in the PVH of male or female mice.
These results suggest that dietary fat may not be the only cause of the previously published changes in hypothalamic connectivity.
Future studies should focus on deciphering the role of individual macronutrients on neuroanatomical and functional changes.