Carotenoids are thought to diminish the incidence of certain degenerative diseases, but the mechanisms involved in their intestinal absorption are poorly understood. Our aim was to obtain basic data on the fate of carotenoids in the human stomach and duodenum. Ten healthy men were intragastrically fed three liquid test meals differing only in the vegetable added 3 wk apart and in a random order. They contained 40 g sunflower oil and mashed vegetables as the sole source of carotenoids. Tomato purée provided 10 mg lycopene as the main carotenoid, chopped spinach (10 mg lutein), and carrot purée (10 mg β-carotene). Samples of stomach and duodenal contents and blood samples were collected at regular time intervals after meal intake. all -trans and ciscarotenoids were assayed in stomach and duodenal contents, in the fat and aqueous phases of those contents, and in chylomicrons. The cis-trans β-carotene and lycopene ratios did not significantly vary in the stomach during digestion. Carotenoids were recovered in the fat phase present in the stomach during digestion. The proportion of all -trans carotenoids found in the micellar phase of the duodenum was as follows (means ± SE): lutein (5.6 ± 0.4%), β-carotene (4.7 ± 0.3%), lycopene (2.0 ± 0.2%). The proportion of 13- cis β-carotene in the micellar phase was significantly higher (14.8 ± 1.6%) than that of the all -trans isomer (4.7 ± 0.3%). There was no significant variation in chylomicron lycopene after the tomato meal, whereas there was significant increase in chylomicron β-carotene and lutein after the carrot and the spinach meals, respectively. There is no significant cis-transisomerization of β-carotene and lycopene in the human stomach. The stomach initiates the transfer of carotenoids from the vegetable matrix to the fat phase of the meal. Lycopene is less efficiently transferred to micelles than β-carotene and lutein. The very small transfer of carotenoids from their vegetable matrices to micelles explains the poor bioavailability of these phytomicroconstituents.

Cardiolipins (CLs) are specific phospholipids of the mitochondria composing about 20% of the inner mitochondria membrane (IMM) phospholipid mass. Dysregulation of CL metabolism has been observed in several types of cancer. In most cases, the evidence for a role for CL in cancer is merely correlative, suggestive, ambiguous, and cancer-type dependent. In addition, CLs could play a pivotal role in several mitochondrial functions/parameters such as bioenergetics, dynamics, mitophagy, and apoptosis, which are involved in key steps of cancer aggressiveness (i.e., migration/invasion and resistance to treatment). Therefore, this review focuses on studies suggesting that changes in CL content and/or composition, as well as CL metabolism enzyme levels, may be linked with the progression and the aggressiveness of some types of cancer. Finally, we also introduce the main mitochondrial function in which CL could play a pivotal role with a special focus on its implication in cancer development and therapy.

Background: Cancer cachexia is a complex syndrome related to a negative energy balance resulting in muscle wasting. Implication of muscle mitochondrial bioenergetics alterations during cancer cachexia was suggested. Therefore, the aim of this study was to explore the efficiency of oxidative phosphorylation in skeletal muscle mitochondria in a preclinical model of cancer cachexia.Methods: Berlin–Druckrey IX rats with peritoneal carcinosis (PC) were used as a model of cancer cachexia with healthy pair‐fed rats (PF) as control. Hindlimb muscle morphology and fibre type composition were analysed in parallel with ubiquitin ligases and UCP gene expression. Oxidative phosphorylation was investigated in isolated muscle mitochondria by measuring oxygen consumption and ATP synthesis rate.Results: PC rats underwent significant muscle wasting affecting fast glycolytic muscles due to a reduction in fibre cross‐sectional area. MuRF1 and MAFbx gene expression were significantly increased (9‐ and 3.5‐fold, respectively) in the muscle of PC compared to PF rats. Oxygen consumption in non‐phosphorylating state and the ATP/O were similar in both groups. Muscle UCP2 gene was overexpressed in PC rats. State III and the uncoupled state were significantly lower in muscle mitochondria from PC rats with a parallel reduction in complex IV activity (−30 %).Conclusion: This study demonstrated that there was neither alteration in ATP synthesis efficiency nor mitochondrial uncoupling in skeletal muscle of cachectic rats despite UCP2 gene overexpression. Muscle mitochondrial oxidative capacities were reduced due to a decrease in complex IV activity. This mitochondrial bioenergetics alteration could participate to insulin resistance, lipid droplet accumulation and lactate production.

Research investigators have shown a growing interest in investigating alterations underlying skeletal muscle wasting in patients with cancer. However, skeletal muscle dysfunctions associated with cancer cachexia have mainly been studied in preclinical models. In the present review, we summarize the results of clinical studies in which skeletal muscle biopsies were collected from cachectic vs. non‐cachectic cancer patients. Most of these studies suggest the presence of significant physiological alterations in skeletal muscle from cachectic cancer patients. We suggest a hypothesis, which connects structural and metabolic parameters that may, at least in part, be responsible for the skeletal muscle atrophy characteristic of cancer cachexia. Finally, we discuss the importance of a better standardization of the diagnostic criteria for cancer cachexia, as well as the requirement for additional clinical studies to improve the robustness of these conclusions.