Bile acids are possible candidate agents in newly identified pathways through which energy expenditure may be regulated. Preclinical studies suggest that
bile acids activate the
enzyme type 2
iodothyronine deiodinase, which deiodinates
thyroxine (T4) to the biologically active
triiodothyronine (T3). We aimed to evaluate the influence of
bile acid exposure and
incretin hormones on thyroid function parameters in patients with
type 2 diabetes.
Thyroid-stimulating hormone (TSH) and
thyroid hormones (total T3 and free T4) were measured in plasma from two human studies: i) 75 g-oral
glucose tolerance test (OGTT) and three isocaloric (500 kcal) and isovolaemic (350 ml) liquid meals with increasing fat content with concomitant ultrasonographic evaluation of gallbladder emptying in 15 patients with
type 2 diabetes and 15 healthy age, gender and BMI-matched controls (meal-study) and ii) 50 g-OGTT and isoglycaemic intravenous
glucose infusions (IIGI) alone or in combination with
glucose-dependent insulinotropic
polypeptide (GIP),
glucagon-like peptide 1 (GLP1) and/or GLP2, in ten patients with
type 2 diabetes (IIGI-study). In both studies, TSH levels declined (P<0.01) similarly following all meal and infusion stimuli. T3 and T4 concentrations did not change in response to any of the applied stimuli. TSH levels declined independently of the degree of gallbladder emptying (meal-study), route of nutrient administration and infusion of gut
hormones. In conclusion, intestinal bile flow and i.v. infusions of the gut
hormones, GIP, GLP1 and/or GLP2, do not seem to affect thyroid function parameters. Thus, the presence of a 'gut-thyroid-pituitary' axis seems questionable.