Primary cilia are organelles that are present on many different cell types, either transiently or permanently. They play a crucial role in receiving signals from the environment and passing these signals to other parts of the cell. In that way, they are involved in diverse processes such as adipocyte differentiation and olfactory sensation. Mutations in genes coding for ciliary proteins often have pleiotropic effects and lead to clinical conditions, ciliopathies, with multiple symptoms. In this study, we reviewed observations from ciliopathies with obesity as one of the symptoms. It shows that variation in cilia-related genes is itself not a major cause of obesity in the population but may be a part of the multifactorial aetiology of this complex condition. Both common polymorphisms and rare deleterious variants may contribute to the obesity risk. Genotype–phenotype relationships have been noticed. Among the ciliary genes, obesity differs with regard to severity and age of onset, which may relate to the influence of each gene on the balance between pro- and anti-adipogenic processes. Analysis of the function and location of the proteins encoded by these ciliary genes suggests that obesity is more linked to activities at the basal area of the cilium, including initiation of the intraflagellar transport, but less to the intraflagellar transport itself. Regarding the role of cilia, three possible mechanistic processes underlying obesity are described: adipogenesis, neuronal food intake regulation and food odour perception.

Pulses are low-glycaemic foods rich in protein (20–25 %), resistant starch and fibre that suppress appetite and glycaemia. The objective of the present study was to elucidate the component(s) of yellow peas responsible for these benefits and assess their efficacy as value-added food ingredients. We investigated the effects of 10 or 20 g of isolated yellow pea protein (P10 and P20) or fibre (F10 and F20) on food intake (FI) at an ad libitum pizza meal served at 30 min (Expt 1, n 19) or 120 min (Expt 2, n 20) and blood glucose (BG) and appetite in young, healthy males (20–30 years). In Expt 1, P20 led to lower FI than control (4937 (sem 502) v. 5632 (sem 464) kJ (1180 (sem 120) v. 1346 (sem 111) kcal)) and all other treatments (P < 0·01) and lower cumulative FI (pizza meal kcal+treatment kcal; CFI) compared to F10 (5460 (sem 498) v. 6084 (sem 452) kJ (1305 (sem 119) v. 1454 (sem 108) kcal); P = 0·033). Both protein treatments suppressed mean pre-meal (0–30 min) BG compared to control (P < 0·05), whereas only P20 suppressed mean post-meal (50–120 min) BG (P < 0·01). There was no effect of treatment on pre-meal or post-meal appetite. In Expt 2, there was no effect of treatment on FI, CFI, or pre- or post-meal BG or appetite. In conclusion, protein is the component responsible for the short-term effects of yellow peas in the regulation of glycaemia and FI, but its second-meal effects disappear by 2 h post-consumption.

More than 70 years ago the glucostatic, lipostatic and aminostatic hypotheses proposed that the central nervous system sensed circulating levels of different metabolites, changing feeding behaviour in response to the levels of those molecules. In the last 20 years the rapid increase in obesity and associated pathologies in developed countries has involved a substantial increase in the knowledge of the physiological and molecular mechanism regulating body mass. This effort has resulted in the recent discovery of new peripheral signals, such as leptin and ghrelin, as well as new neuropeptides, such as orexins, involved in body-weight homeostasis. The present review summarises research into energy balance, starting from the original classical hypotheses proposing metabolite sensing, through peripheral tissue–brain interactions and coming full circle to the recently-discovered role of hypothalamic fatty acid synthase in feeding regulation. Understanding these molecular mechanisms will provide new pharmacological targets for the treatment of obesity and appetite disorders.

In a randomised, single blind, placebo-controlled crossover design study, we investigated whether healthy, non-smoking, dietary unrestrained women (n 24), divided into linoleic acid tasters (LAT, n 14) and linoleic acid non-tasters (LANT, n 10), differed in food intake regulation when linoleic acid was added to ice creams. The determination of subjects as LAT or LANT was done using a 10μM-linoleic acid solution. The ice creams were characterised by the subjects and a taste perception test using the triangle test was conducted three times. Food intake and appetite were measured using the universal eating monitor. LAT and LANT did not differ in characterisation or in taste perception of the ice creams, even though LAT were able to increase their ability to discriminate between the ice cream with linoleic acid from the one containing oleic acid. No effect of LAT status or type of ice cream was found for hedonic value of the ice creams. Linoleic acid taster status did affect food intake regulation. For LAT, but not LANT, the amount eaten was a function of Δsatiety. Subjects ate by weight of food and not by energy content. In conclusion, differences in food intake regulation were seen between LAT and LANT, in that the amount eaten by LAT was a function of Δsatiety, but was not for LANT.

The aim of the present study was to investigate associations between spontaneous meal initiations and blood glucose dynamics in overweight male subjects in negative energy balance. In a randomized crossover design, fifteen overweight male subjects (BMI 28·6 (SD 1·8 kg/m2) participated in three treatments, each of which consisted of 2 weeks consuming a low-energy diet followed by a test of voluntary food ingestion in the absence of time-related cues. The low-energy diet consisted of three daily meals (947 kJ) which were either semi-solid with or without 2·5 g guar gum, or solid, and a dinner of subject's own choice. During the time-blinded test, on the first, second, and third meal initiation subjects ingested a low-energy meal corresponding to that used during the preceding weeks. Changes in blood glucose were monitored on-line. Associations between spontaneous meal initiations and blood glucose dynamics were determined using the χ2 test. No difference was found between treatments in the occurrence of postabsorptive and postprandial declines in blood glucose or in associations between meal initiations and blood glucose dynamics. Postprandial dynamic blood glucose declines were associated with meal initiation (χ2 26·8, P<0·001), but postabsorptive and postprandial transient declines were not. In overweight subjects, the usual association between transient declines and spontaneous meal initiation was completely absent in negative energy balance.

In a study of the impact of aspartame, fat, and carbohydrate on appetite, we monitored blood glucose continuously for 431 (se 16) min. Ten healthy males (19–31 years) participated in three time-blinded visits. As blood glucose was monitored, appetite ratings were scored at randomized times. On the first meal initiation, volunteers consumed one of three isovolumetric drinks (aspartame, 1 MJ simple carbohydrate, and 1 MJ high-fat; randomized order). High-fat and high-carbohydrate foods were available ad libitum subsequently. Blood glucose patterns following the carbohydrate drink (+1·78 (se 0·28) mmol/l in 38 (se 3) min) and high-fat drink (+0·83 (se 0·28) mmol/l in 49 (se 6) min) were predictive of the next intermeal interval (R 0·64 and R 0·97 respectively). Aspartame ingestion was followed by blood glucose declines (40 % of subjects), increases (20 %), or stability (40 %). These patterns were related to the volunteers' perception of sweetness of the drink (R 0·81, P = 0·014), and were predictive of subsequent intakes (R -0·71, P = 0·048). For all drinks combined, declines in blood glucose and meal initiation were significantly associated (χ2 16·8, P < 0·001), the duration of blood glucose responses and intermeal intervals correlated significantly (R 0·715, P = 0·0001), and sweetness perception correlated negatively with hunger suppression (R -0·471, P = 0·015). Effects of fat, carbohydrate, and aspartame on meal initiation, meal size, and intermeal interval relate to blood glucose patterns. Varied blood glucose responses after aspartame support the controversy over its effects, and may relate to sweetness perception.