Hypothalamic Inflammation and Glioses as Aetiopathogenetic Factor in High Fat Diet Induced Obesity and Various Therapeutic Options to Resolve it

Abstract

We reviewed the literature relating to hypothalamic inflammation (HI); gliosis in relation
to high-fat diet (HFD) and that how this could be reversed with various types of therapies.
We searched PubMed articles with the MeSH terms “hypothalamic inflammation”, “gliosis”,
“HFD”, “obesity”, and “treatments” used. During HFD intake, we found that the ventromedial
hypothalamus (VMH) astrocytes uses fatty acids (FA’s) to generate ketone bodies which are
then exported to neurons where they produce excess adenosine triphosphate (ATP) and reactive oxygen species (ROS), which overrides CD36 mediated FA sensing and role of astrocytederived ketone bodies in reducing calorie intake in diet resistant but not diet-induced obese
strains was emphasized. The further role of HAM-RS2-a special starch, resolvins abscisic acid,
KBH1, unsaturated fatty acid receptor targeting GPR120/GPR40. Hepatic clock genes were
effective in tackling obesity. We found that in rodents hypothalamic inflammation and glioses
were found to occur immediately with HFD consumption before any significant weight gain.
Sensitivity or resistance to diet-induced obesity in rodents also correlates with the presence or
absence of hypothalamic inflammation and reactive glioses. Further functional interventions
with the increase or decrease inflammation in neurons and glia alter diet associated weight gain.
Various human magnetic resonance imaging (MRI) studies have found glioses and disrupted
connectivity in obese humans. Various factors which can be used to tackle obesity like HAMRS2-a special starch, resolvins, abscisic acid, KBH1, unsaturated fatty acid receptors, GPR120
and GPR40 are some of the explored routes by which these pathways may be explored to
prevent the further extension of the HFD and one may get newer answers for arresting obesity
development.