Physiology of Nutrition and Food Behavior

The number of aesthetic procedures performed worldwide continues to grow together with an increase in the population seeking the restoration or preservation of a youthful appearance. Requests for non-surgical body rejuvenation are increasing. Patients are looking for safe and effective minimally invasive aesthetic procedures. Soft-tissue dermal fillers can meet these expectations. Based on the beneficial outcomes of these treatments in many facial areas, a new trend is developing to target body areas. Different dermal fillers are available and include collagen stimulators initially developed to restore facial volume. Furthermore, they are associated with long-lasting efficiency, a high level of patient satisfaction and a good safety profile, with mainly minor adverse events reported. In appropriate conditions of use, they are now used for body rejuvenation in clinical practice. Their use is expanding and allows addressing various issues including volume loss, skin laxity, cellulite, striae distensae and wrinkles. This review focuses on poly-L-lactic acid (PLLA), used in the first collagen stimulator and one of the most investigated in facial and in off-facial body applications. The available published data, although still limited, are presented by body area, neck and chest, buttocks, abdomen, upper arms, thighs, knees, and hands. Key features of the concerned zones and the main clinical signs affecting the body part as well as the injection modalities are provided along with the aesthetic results. This represents the state of the art on which to base further developments necessary for optimal and safe outcomes of treatment with the PLLA-based collagen stimulators and others in this class for body rejuvenation.

BackgroundAging signs can be corrected through volume restoration in multiple soft tissue layers and in the supraperiosteal plane using hyaluronic acid (HA) or nonhyaluronic acid (non‐HA) fillers. The non‐HA bioresorbable polycaprolactone (PCL)‐based filler with collagen‐stimulating properties has a proven safety profile, but rare potential complications such as nodules and granuloma can occur. Furthermore, PCL‐based fillers cannot be immediately removed by injection of an enzyme. These potential drawbacks have yet to be described in the literature.AimsThe author performed 1111 treatments between 2015 and 2018. This study aims to review and analyze these treatments to ascertain the complication rates of the PCL‐based filler. Suggestions for complication prevention and management are also discussed.Methods780 patients treated with the PCL‐based filler were reviewed by the physician between April 2015 and May 2018. During this period, 5595 syringes were used in 1111 treatments. All complication data were acquired by phone interviews, reports by patients, or observation at follow‐up visits. Complications were subdivided into early‐onset (occurring up to 2 weeks after treatment) and late‐onset events (occurring more than 2 weeks to years after treatment).ResultsAmong the 1111 treatments, there were 50 cases (4.5%) of edema that lasted longer than 2 weeks, 30 cases (2.7%) of bruising, 8 cases (0.72%) of malar edema, 5 cases (0.45%) of temporarily palpable lumps and 2 cases (0.18%) of discoloration. There were no cases of intravascular injection, nodules/granulomas, or infection.ConclusionThe complication rate of the PCL‐based filler was found to be low, and there were no cases of intravascular injection, nodules, and/or granulomas during the 3‐year observation. Longer‐lasting edema was associated with a higher injection volume and malar edema was related to lymphatic compression.

The protein content of the diet has long been investigated for its influence on food behavior. High-protein diets promote satiety and reduce calorie intake, whereas results for low-protein diets are more contradictory and less established. Protein sensing might take place in the oral cavity or in the post-oral gastrointestinal tract, where specific receptors have been found. Protein signaling to the brain may act through the vagal nerve and involve gastric hormones, such as cholecystokinin and peptide YY. Other pathways are post-absorptive signaling and the direct influence of brain levels of amino acids. High-protein diet enhances the activity of brain satiety centers, mainly the nucleus of the solitary tract and arcuate nucleus, although the activity of brain reward centers might also be modified. A better understanding of the role of both homeostatic and hedonic systems is needed to fully describe the influence of protein on food intake.

Recent advances highlight that nutrient receptors (such as T1R1/T1R3 heterodimer, Ca sensing receptor and GPR93 for amino acids and protein, GPR40, GPR41, GPR43 and GPR120 for fatty acids, T1R2/T1R3 heterodimer for monosaccharides) are expressed in the apical face of the gut and sense nutrients in the lumen. They transduce signals for the regulation of nutrient transporter expressions in the apical face. Interestingly, they are also localised in enteroendocrine cells (EEC) and mainly exert a direct control on the secretion in the lamina propria of gastro-intestinal peptides such as cholecystokinin, glucagon-like peptide-1 and peptide YY in response to energy nutrient transit and absorption in the gut. This informs central nuclei involved in the control of feeding such as the hypothalamus and nucleus of the solitary tract of the availability of these nutrients and thus triggers adaptive responses to maintain energy homoeostasis. These nutrient receptors then have a prominent position since they manage nutrient absorption and are principally the generator of the first signal of satiation mechanisms mainly transmitted to the brain by vagal afferents. Moreover, tastants are also able to elicit gut peptides secretion via chemosensory receptors expressed in EEC. Targeting these nutrient and tastant receptors in EEC may thus be helpful to promote satiation and so to fight overfeeding and its consequences.

O efeito do t10,c12-C18:2 na producao de leite e no perfil em acidos graxos (AG) da gordura do leite foi estudado em oito cabras que receberam t10,c12-C18:2 por infusao duodenal (acido linoleico conjugado -CLA, 2g/10 h) durante tres dias, seguido por dois dias de infusao de leite desnatado (SM). As cabras foram distribuidas em quatro grupos em um delineamento fatorial 2x2: duas porcentagens de concentrado da dieta - L, baixa 45% ou H, alta 65% - e dois tipos de gordura adicionada para modificar a relacao c9,c12-C18:2/c9-C18:1 da dieta - graos de soja ou de canola. Amostras de leite foram coletadas antes (basal) e durante a infusao de CLA e de leite desnatado. Ingestao de materia seca, teor e producao de gordura, de proteina e de lactose foram semelhantes antes do inicio e durante a infusao de CLA. A proporcao de AG saturados com 4 a 8C ou 10 a 15C nao foi alterada durante a infusao de CLA. Independentemente da alimentacao das cabras, a infusao de CLA aumentou as proporcoes de C18:0, t10- e t11-C18:1 e diminuiu as de c9-C18:1 e c9,t11-C18:2 na gordura do leite. O CLA diminuiu as relacoes c9-C18:1/C18:0 e c9,t11-C18:2/t11-C18:1 no leite dos quatro grupos experimentais. Os resultados mostraram que a lipogenese mamaria em cabras leiteiras nao foi alterada por 2g/d de t10,c12-C18:2, contudo, a desaturacao de AG de cadeia longa parece ser diminuida da mesma maneira que em vacas. Producao de leite e perfil dos AG do leite nao foram influenciados pela relacao c9,c12-C18:2/c9-C18:1 da fracao lipidica da dieta das cabras.

Butyrate and acetate are bacterial metabolites present in the large intestine lumen. Although butyrate is well known to inhibit the in vitro proliferation of human colon carcinoma cells in a process involving the hyperacetylation of specific nuclear histones, little is known about the possible link between butyrate metabolism and its growth-inhibitory effect. In a previous study (Leschelle et al., 2000, Eur J Biochem 267: 6435-6442), we showed that butyrate accumulates and is metabolized in HT-29 Glc(-/+) cells without increasing oxygen consumption. In the present study, using the same cell line incubated with (14)C-labeled butyrate, we determined that a minor part of (14)C from butyrate was recovered in nuclear histones. Unlike butyrate, acetate exerted no effect on cell growth but was a precursor for overall net histone acetylation. Although butyrate was able to increase the cellular AMP/ADP ratio, it did not affect the ATP cell content or the adenylate charge or the oxidation of endogenous L-glutamine. Butyrate oxidation was found to be markedly sensitive to the presence of other substrates with D-glucose decreasing this oxidation and L-malate stimulating it. Furthermore, in the presence of L-malate, the growth-inhibitory effect of butyrate was significantly weaker than in its absence. From these data, we conclude that the metabolism of butyrate downstream acetyl-CoA synthesis is not involved in the butyrate antiproliferative effect. The suggestion that butyrate metabolism in mitochondria is not used in these cells as a fuel but acts as a regulator of butyrate free concentrations (thus limiting its action upon cellular targets), is discussed.