Hormonal Modulation of Fat Mass Induced Insulin Resistance.

Each unit increase in BMI was associated with approximately a 2% decline in HOMA-S and a 1% rise in HOMA-B.

• A strong, linear dose-response relationship was found between BMI and HOMA indices.
• Analysis was conducted using adjusted multivariable linear regression.
• The study population consisted of 289 adults without diabetes from Hamad General Hospital in Qatar.
• Participants had obesity but were without diabetes.

Hormonal variations, particularly leptin and GIP levels, more strongly predicted insulin sensitive phenotype (ISP) than BMI alone.

• Subgroup analysis revealed that effects on ISP were more strongly driven by hormonal variations than by BMI alone.
• A logistic regression model was used to investigate hormonal predictors of ISP.
• Results were presented using margins plots, stratified by obesity classes.
• The key hormones investigated were leptin and gastric inhibitory peptide (GIP).

BMI was found to function as a proxy for hormonal variations, particularly in leptin and GIP, in relation to insulin sensitivity.

• The association of leptin and GIP with both HOMA indices and BMI was investigated.
• The study was cross-sectional in design, involving 289 adults without diabetes.
• Findings support the need for incorporating hormonal markers into obesity-related risk assessment and management strategies.
• Participants were recruited from Hamad General Hospital in Qatar.

The study identified a relationship between BMI and pancreatic β-cell function as measured by HOMA-B.

• HOMA-B (homeostatic model assessment for pancreatic β-cell function) was analyzed alongside HOMA-S.
• Each unit increase in BMI was linked to approximately a 1% rise in HOMA-B.
• Both HOMA-S and HOMA-B were analyzed as outcomes using adjusted multivariable linear regression with BMI as a predictor.
• The dose-response relationship between BMI and HOMA-B was described as strong and linear.