Although UHT heat treatment is being optimized to improve the stability and functional properties of dairy products, its metabolic effects remain scarcely known. As such, we studied the effect of the type of UHT process on lipid metabolism, intestinal barrier, and inflammation in mice. Nine-week-old male C57Bl/6J mice were fed a diet composed of nonlipidic powder mixed with different UHT dairy creams (final: 13% milkfat) for 1 or 4 wk. All creams contained 0.02% of thickener (carrageenan) and were treated via either (1) classical indirect heating process (Th), (2) indirect process at higher temperature (Th+), or (3) direct process by steam injection (ThD). Plasma, epididymal adipose tissue (EAT), and intestine were analyzed. Multivariate principal component analyses were used to identify differential effects of processes. Th+ differed by a globally higher liver damage score compared with that of the other creams. After 4 wk, the duodenal expression of lipid absorption genes fatty acid binding protein 4 (Fatp4) and microsomal triglycerides transfer protein (Mttp) was lower in the Th+ versus Th group. Expression in the colon of tight junction protein zonula occludens 1 (Zo1) and of some endoplasmic reticulum stress markers was lower in both Th+ and ThD versus the Th group. In EAT, ThD had lower gene expression of several inflammatory markers after 4 wk. Some differential effects may be related to heat-induced physicochemical changes of creams. The type of cream UHT process differentially affected metabolic parameters in mice after a 4-wk fat-rich diet, partly due to cream structure. Altogether, direct steam injection process induced the lowest early markers of high-fat-induced metabolic inflammation in EAT.

Additives stabilize or improve the organoleptic or functional properties (or both) of many dairy products including whipping cream. Their influence on the metabolic effect of dairy cream is scarcely known. We tested the hypothesis that added emulsifier (lactic acid esters of mono-and diglycerides; MAG/DAG), thickener (carrageenan, CGN), or both, could modify the metabolic effect, notably in the intestine and liver. Nine-week-old male C57Bl/6J mice were fed UHT cream (indirect treatment) mixed with nonlipidic powder (final: 13% milkfat) for 1 or 4 wk. We compared creams (1) without additive (Ctl), (2) with thickener (Th), 0.02% of κ-CGN, and (3) with both thickener and emulsifier, 0.1% of MAG/DAG esters (Th/Em). We analyzed plasma parameters, intestine, and liver. Fasting glycemia, insulinemia, triglyceridemia, nonesterified fatty acids, body weight gain, and liver weight did not differ among groups. After 1 wk, Th/Em had higher expression in the duodenum of some of the genes involved in (1) intestinal lipid absorption and (2) tight junction proteins versus Ctl and Th. After 4 wk, mucus cell number in the small intestine was higher in Th/Em versus Ctl and Th. Genes involved in endoplasmic reticulum (ER) stress in the duodenum were more expressed in Th/Em after 1 wk. After 4 wk, in the colon, a higher expression of ER stress genes was observed for Th versus Th/Em and Ctl. Liver damage score was not altered by additives. Adding both CGN (0.02%) and MAG/ DAG esters (0.1%) in dairy cream did not result in deleterious outcomes in mice after 4 wk regarding lipid metabolism, intestinal permeability, and liver disorders. The longer term effect of intestinal ER stress modulation deserves further investigation.