Childhood Obesity, Hypothalamic Inflammation, and the Onset of Puberty: A Narrative Review.
Anastasia-Maria TzounakouGalateia StathoriGeorgios PaltoglouGeorgios ValsamakisMastorakos GeorgeNikolaos F VlahosEvangelia CharmandariPublished in: Nutrients (2024)
The onset of puberty, which is under the control of the hypothalamic-pituitary-gonadal (HPG) axis, is influenced by various factors, including obesity, which has been associated with the earlier onset of puberty. Obesity-induced hypothalamic inflammation may cause premature activation of gonadotropin-releasing hormone (GnRH) neurons, resulting in the development of precocious or early puberty. Mechanisms involving phoenixin action and hypothalamic microglial cells are implicated. Furthermore, obesity induces structural and cellular brain alterations, disrupting metabolic regulation. Imaging studies reveal neuroinflammatory changes in obese individuals, impacting pubertal timing. Magnetic resonance spectroscopy enables the assessment of the brain's neurochemical composition by measuring key metabolites, highlighting potential pathways involved in neurological changes associated with obesity. In this article, we present evidence indicating a potential association among obesity, hypothalamic inflammation, and precocious puberty.
Keyphrases
- weight loss
- metabolic syndrome
- insulin resistance
- type diabetes
- high fat diet induced
- weight gain
- oxidative stress
- bariatric surgery
- adipose tissue
- induced apoptosis
- white matter
- mass spectrometry
- ms ms
- gene expression
- cerebral ischemia
- human health
- multiple sclerosis
- photodynamic therapy
- signaling pathway
- cell cycle arrest
- inflammatory response
- genome wide
- physical activity
- endothelial cells
- neuropathic pain
- obese patients