Decrease in leptin mediates rat bone metabolism impairments during high-fat diet-induced catch-up growth by...

Area of Science:

• Endocrinology
• Bone Biology
• Metabolic Research

Background:

• Catch-up growth (CUG) has known adverse health effects, but its impact on bone metabolism remains under-investigated.
• High-fat diets (HFD) are a common trigger for CUG, necessitating research into associated metabolic consequences.
• Leptin's role in bone metabolism during CUG requires clarification, particularly in the context of HFD.

Purpose of the Study:

• To investigate the effects of leptin on bone metabolism and formation during high-fat diet-induced catch-up growth.
• To elucidate the mechanisms involving leptin, osteoprotegerin (OPG), and receptor activator of nuclear factor-kappa b ligand (RANKL) in HFD-induced CUG bone changes.

Main Methods:

• Male Wistar rats were divided into control, caloric restriction/normal chow, caloric restriction/HFD, and HFD/leptin antagonist groups.
• Body weight, biochemical markers, and adipose tissue were monitored.
• Bone metabolism was assessed using Hematoxylin and Eosin (H&E) staining, qRT-PCR, and immunohistochemistry for OPG and RANKL.

Main Results:

• HFD significantly increased body weight and adipose tissue accumulation.
• Bone metabolism markers were significantly altered in the caloric restriction/HFD and HFD/leptin antagonist groups.
• HFD-induced CUG led to severe bone formation impairment, exacerbated by a leptin antagonist, with decreased OPG and increased RANKL expression.

Conclusions:

• High-fat diet-induced catch-up growth significantly impairs bone formation.
• Leptin plays a crucial role in regulating bone metabolism during HFD-induced CUG, mediated by OPG and RANKL.
• Leptin antagonism during CUG further aggravates bone loss, highlighting leptin's protective role in bone health under these conditions.