PNAS: Obesity, diabetes is "girls and boys"! When neurons are damaged, female metabolism is abnormal and male is not.

Sugars, fats, and proteins are the main sources of energy that sustain our lives, and the body's intake and use of these substances is a complex and sophisticated process.
errors in this process can lead to metabolic imbalances in the body that could eventually lead to diseases such as obesity or diabetes. the
-abdominal heotynachosis (VMH) plays a major role in glucose/lipid stabilization, and in mammalian VMH neurons that sense metabolic stability, such as steroid-producing factor 1 (SF1) neurons, regulate glucose and lipid levels.
previous study found higher concentrations of estrogen receptor 2 in VMH.
, does this mean that estrogen plays a more important role in regulating certain metabolisms? Recently, an article published in PNAS called "Essential sex-specific effects of mGluR5 in ventromedial hypothalamus regulation estrogen signaling and glucose balance" revealed for the first time that in the absence of glutamate receptacle 5 sub-type (mGluR5), the activity of SF1 neurons in female mice is disrupted and the protective effect of estrogen on glucose metabolism can be reversed.
addition, the researchers speculate that this reverse effect of estrogen on glucose metabolism may explain why post-menopoly women are more likely to have insulin resistance and an increased risk of diabetes.
neurons are present in the inner heotrhea (VMH) of the abdomen, where structural and functional changes occur in the stress state (external/internal stimulation).
Metabolic glutamate receptacle 5 subtope (mGluR5) play an important role in regulating the connection between neurons and neurons, and the function of mGluR5 in certain areas of the brain is regulated by brain-based neurotrophic factors (BDNF).
Previous studies have found that decreased excitability of neurons causes over-eating, glucose intolerance, and obesity in mice with female BDNF2L/2LCk cre mutants (BDNF deficiency causes damage to the center).
and mGluR5 is so important to neurons, what are the consequences of the absence of mGluR5? First, the researchers used male and female BDNF2L/2LCk cre mutant mice for the relevant experiments, and found that the expression of mGluR5 in these mutant mice decreased.
when the researchers used gene editing to knock out mGluR5, they observed an abnormal reversal of normal glucose/lipid levels in female mice.
most surprising of all, abnormal glucose/lipid metabolism occurred only in female mice.
metabolism of glucose/lipids in male mice missing mGluR5 remained normal.
so, what is the reason for this phenomenon of "son-in-arms"? Next, the team looked at hormones in the serum of female and male BDNF2L/2LCk cre mutant mice and found that levels of nodepine in the serum of female mutants decreased significantly, but there was no effect in male mutants, suggesting that reduced intersysitone nerve tension caused this "gender difference."
In turning out, the team further examined the relationship between the discharge rate of neurons and blood sugar metabolism and found that estrogen had significantly different effects on SF1 neuron activity and blood sugar metabolism with or without mGluR5, without which estrogen inhibited SF1 neuron activity and regulated blood sugar from normal to abnormal, without which no changes were observed in male mutants.
In summary, the study found that glutamate receptacle 5 (mGluR5) is essential for estrogen to regulate estrogen-regulated glucose levels, and that there does not appear to be any effect in males, which will help us better understand why men and women have different risks of diabetes or other diseases throughout their lives.
Moreover, since estrogen play an important role in regulating a woman's blood sugar/lipid metabolism, can a woman properly add natural estrogens (such as estrogen in plants) after menoopone to maintain certain metabolic stability? It will all be worth thinking about further.
.