ABSTRACT
A preference for chili pepper can be an acquired taste. The contrast between a chili lover and a hater illustrates the complexities involved in forming an appreciation for food that evokes a fiery pain sensation. This narrative review aims to understand the factors behind chili pepper preference formation across the life course and how individual chili pepper preferences can impact eating behaviors and dietary intake. This review was conducted using three databases, yielding 38 included articles. Results suggest five determinants of chili pepper preferences: culture, exposure, gender, genetics, and personality. Collective findings indicate that the strongest influences on preference acquisition include the individual environment from childhood to adulthood and repeated exposure to spicy flavors. With frequent exposure to spicy food, the perceived burn becomes less intense. Culture also influences exposure to chili peppers, with the highest consumption patterns seen within Mexico and some Asia countries. Additionally, males reported having a stronger preference for spicy foods than females. Twin studies illustrated that genetics influenced spicy taste preferences, underscoring the complexity of developing individual taste preferences. As for the impact of capsaicin-containing food on individual eating behaviors and dietary behaviors, appetite effects depend on the dose of capsaicin consumed, but three studies found a change in sensory desires for sweet and fatty foods after finishing a capsaicin-containing dish. Inconsistent results were reported for chili pepper's effects on hunger and satiety after consumption, but changes in specific food desires were observed. The impact of chili pepper on appetite and calories consumed was inconsistent, but the greater amount of capsaicin ingested, the greater the effect. Capsaicin's potential to be used for weight control needs to be further reviewed. In conclusion, evidence suggests that chili pepper preferences may be linked to innate and environmental aspects such as an individual's culture, gender, and genetics. Extrinsic factors like repeated exposure may increase the liking for spicy foods.
ABSTRACT
Fenofibrate slows the progression of clinical diabetic retinopathy (DR), but its mechanism of action in the retina remains unclear. Fenofibrate is a known agonist of peroxisome proliferator-activated receptor alpha (PPARα), a transcription factor critical for regulating metabolism, inflammation and oxidative stress. Using a DR mouse model, db/db, we tested the hypothesis that fenofibrate slows early DR progression by activating PPARα in the retina. Relative to healthy littermates, six-month-old db/db mice exhibited elevated serum triglycerides and cholesterol, retinal gliosis, and electroretinography (ERG) changes including reduced b-wave amplitudes and delayed oscillatory potentials. These pathologic changes in the retina were improved by oral fenofibrate. However, fenofibrate did not induce PPARα target gene expression in whole retina or isolated Müller glia. The capacity of the retina to respond to PPARα was further tested by delivering the PPARα agonist GW590735 to the intraperitoneal or intravitreous space in mice carrying the peroxisome proliferator response element (PPRE)-luciferase reporter. We observed strong induction of the reporter in the liver, but no induction in the retina. In summary, fenofibrate treatment of db/db mice prevents the development of early DR but is not associated with induction of PPARα in the retina.
ABSTRACT
Adropin is a peptide hormone encoded by the Energy Homeostasis Associated (ENHO) gene whose physiological role in humans remains incompletely defined. Here we investigated the impact of dietary interventions that affect systemic glucose and lipid metabolism on plasma adropin concentrations in humans. Consumption of glucose or fructose as 25% of daily energy requirements (E) differentially affected plasma adropin concentrations (P < 0.005) irrespective of duration, sex or age. Glucose consumption reduced plasma adropin from 3.55 ± 0.26 to 3.28 ± 0.23 ng/ml (N = 42). Fructose consumption increased plasma adropin from 3.63 ± 0.29 to 3.93 ± 0.34 ng/ml (N = 45). Consumption of high fructose corn syrup (HFCS) as 25% E had no effect (3.43 ± 0.32 versus 3.39 ± 0.24 ng/ml, N = 26). Overall, the effect of glucose, HFCS and fructose on circulating adropin concentrations were similar to those observed on postprandial plasma triglyceride concentrations. Furthermore, increases in plasma adropin levels with fructose intake were most robust in individuals exhibiting hypertriglyceridemia. Individuals with low plasma adropin concentrations also exhibited rapid increases in plasma levels following consumption of breakfasts supplemented with lipids. These are the first results linking plasma adropin levels with dietary sugar intake in humans, with the impact of fructose consumption linked to systemic triglyceride metabolism. In addition, dietary fat intake may also increase circulating adropin concentrations.
