Obesity Research Highlights Recent Findings on Leptin and Cardiac Function

Recent studies from the United States and Canada have shed new light on the relationship between obesity, cardiac function, and leptin. Research has shown that leptin-deficient and leptin-resistant mice experience increased apoptosis, DNA damage, and mortality compared to their wild-type counterparts. Furthermore, studies have found that leptin induces rat glomerular mesangial cell hypertrophy, but does not regulate hyperplasia or apoptosis. Additionally, a study comparing two exercise training programs on cardiac responsiveness to beta-stimulation in obesity found that increased training volume failed to attenuate obesity-related decrements in isolated heart responsiveness to beta-adrenergic stimulation.

Key Takeaways:

• Leptin-deficient and leptin-resistant mice exhibit increased apoptosis, DNA damage, and mortality compared to wild-type mice, suggesting that normal leptin signaling is necessary to prevent excess age-associated DNA damage and premature mortality (Barouch et al., 2006).
• Leptin induces rat glomerular mesangial cell hypertrophy, but does not regulate hyperplasia or apoptosis, which may play a role in the pathophysiology of nephropathy associated with obesity (Lee et al., 2005).
• Increased training volume in exercise training programs did not attenuate obesity-related decrements in isolated heart responsiveness to beta-adrenergic stimulation, and instead caused reduced sensitivity to isoproterenol in both lean and obese animals (Carroll et al., 2005).
• The hypertrophic effect of leptin may play a role in the pathophysiology of nephropathy associated with obesity, and further research is needed to understand the mechanisms underlying this relationship.
• Exercise training did not restore normal cardiac beta-adrenergic responsiveness in obese rabbits, highlighting the complex relationship between exercise and cardiac function in obesity (Carroll et al., 2005).

Statistics:

• 33% increase in cell size and 40% increase in leucine incorporation in rat glomerular mesangial cells treated with leptin (Lee et al., 2005).
• 27% increase in total treadmill work over 12 weeks for obese animals trained with increased training volume (Carroll et al., 2005).
• 1-way analysis of variance and Tukey's post-hoc test were used to compare controls with animals trained under low- and high-training volume programs.
• Concentration-response data were fit to a sigmoidal function using a four-parameter logistic equation to study developed pressure, +dP/dt[subscript]max, and -dP/dt[subscript]max responses to isoproterenol.

Sources:

• Barouch et al. (2006). Cardiac myocyte apoptosis is associated with increased DNA damage and decreased survival in murine models of obesity. Circ Res, 98(1), 119-124.
• Lee et al. (2005). Leptin induces rat glomerular mesangial cell hypertrophy, but does not regulate hyperplasia or apoptosis. Int J Obes, 29(12), 1395-1401.
• Carroll et al. (2005). A comparison of two exercise training programs on cardiac responsiveness to beta-stimulation in obesity. Exp Biol Med, 230(3), 180-188.