A carnosine intervention study in overweight human volunteers: bioavailability and reactive carbonyl species sequestering effect

Abstract

Carnosine is a natural dipeptide able to react with reactive carbonyl species, which have been recently associated with the onset and progression of several human diseases. Herein, we report an intervention study in overweight individuals. Carnosine (2 g/day) was orally administered for twelve weeks in order to evaluate its bioavailability and metabolic fate. Two carnosine adducts were detected in the urine samples of all subjects. Such adducts are generated from a reaction with acrolein, which is one of the most toxic and reactive compounds among reactive carbonyl species. However, neither carnosine nor adducts have been detected in plasma. Urinary excretion of adducts and carnosine showed a positive correlation although a high variability of individual response to carnosine supplementation was observed. Interestingly, treated subjects showed a significant decrease in the percentage of excreted adducts in reduced form, accompanied by a significant increase of the urinary excretion of both carnosine and carnosine-acrolein adducts. Altogether, data suggest that acrolein is entrapped in vivo by carnosine although the response to its supplementation is possibly influenced by individual diversities in terms of carnosine dietary intake, metabolism and basal production of reactive carbonyl species.

Identification and characterisation of carnostatine (SAN9812), a potent and selective carnosinase (CN1) inhibitor with in vivo activity

“…Other human trials have shown a positive effect of carnosine supplementation on insulin sensitivity in obese human individuals Regazzoni et al 2016). Because of the reasons given above, an additional CN1 inhibition may further increase these beneficial effects.…”

The effect of 12 weeks carnosine supplementation on renal functional integrity and oxidative stress in pediatric patients with diabetic nephropathy: a randomized placebo‐controlled trial

“…Planned duration of the treatment with carnosine was 12 weeks as previously reported [31][32][33] was considered if <80% of the study medication and ACE inhibitors had been taken. 34 The primary study endpoint was the change in A1M after the 12 weeks of treatment among diabetic patients receiving carnosine when compared to the placebo group.…”

Multitarget trehalose-carnosine conjugates inhibit Aβ aggregation, tune copper(II) activity and decrease acrolein toxicity

“…[12,39,40,] ACR is one of the most harmful aldehydes; in humans, ACR can be formed endogenously by amine oxidation or metabolism reactions of amino acids; environmental pollution and oxidative reactions in food preparations are the main sources of exogenous ACR. [41] The involvement of Car in the detoxification process of ACR has recently been proved both in mice and humans. [ 42 ] Based on the above, the ability of trehalosecarnosine conjugates (TrCar1 and TrCar2) to react with ACR was tested and compared to that of underivatized Car.…”