Caffeine and Type 2 Diabetes - Caffeine: Chemistry, Analysis, Function and Effects - page 375

of pancreatic b-cells (Kagami et al 2008). One recent study in rats reported that
caffeine may protect pancreatic b-cells against natural toxins such as
streptozotocin (Kagami et al 2008). Moreover, several studies have shown
that caffeine increases resting metabolic rate (Astrup et al 1990) and decreases
body weight (Boozer et al 2002). In addition, studies have shown that after
ingestion of caffeine (10mg kg 21 ), lipid turnover increases by 2-fold. Also,
thermic changes (13.3% increase), oxidative free fatty acids (FFA) disposal
(44% increase), and non-oxidative FFA disposal (2.3-fold increase) were
observed (Acheson et al 2004). Interestingly, it has been reported that the
inverse association of coffee intake with T2D risk only applied to those who
had previously lost weight (Greenberg et al 2005). Further, a prospective
cohort study conducted in United States examined a relation between caffeine
intake and 12-year weight change. The authors reported that participants who
increased their caffeine consumption had lower mean body gain than those
who decreased their caffeine consumption in both men and women (Lopez-
Garcia et al 2006). These findings suggest the crucial role of weight loss in
relating coffee intake to T2D risk.
It is important to note that several experimental studies indicated that caffeine
may acutely impair insulin sensitivity. In a cross-over study, caffeinated-coffee
consumption for 4 weeks increased fasting insulin levels compared with coffee
abstinence, but did not reduce fasting glucose levels, raising concern of the acute
impairment of insulin sensitivity (van Dam et al 2004). It is considered that
caffeine acutely decreases insulin sensitivity in skeletal muscle via antagonism of
adenosine A1 receptors in skeletal muscle and increasing sympathetic activity.

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Figure 20.1

Potential mechanisms for the relation between long-term caffeine intake
and type 2 diabetes risk.