Animals and treatments 
 
 Animal experiments were performed at Imperial College London except for high resolution magic angle spinning (HMRS) experiments which were performed at Instituto de Investigaciones Biomédicas ‘Alberto Sols’ (IIB). Experiments conducted at Imperial College London were approved by Imperial College London, and all animal procedures were performed in accordance with the UK Animals Scientific Procedures Act (1986). IIB experiments were approved by the ethical committee of the Instituto de Investigaciones Biomedicas ‘Alberto Sols’ (and met the guidelines of the national (R.D. 53/2013) and the European Community (2010/62/UE) for care and management of experimental animals. Unless otherwise stated, all experiments were performed in C57BL/6 male mice (6–8 weeks old, Charles River, Margate, UK) that were single-housed under controlled temperature (21–23 oC) and light conditions (12 h light–dark cycle; lights on at 07:00 hours). 
 
 The effect of HF-I versus HF-C on body weight and energy intake 
 
 Mice were randomized and assigned to two different groups (n=12): HFD with cellulose as a control (HF-C), HFD+oligofructose-enriched inulin (Synergy) (HF-I). Synergy is a fructan-based preparation containing both long- and short-chain fructo-oligosaccharides. Synergy was mixed with the HFD individually in the ratio of 1:9. The two diets were isocaloric, each contained the same total energy of 4.6 kcal g−1, with 41.8% energy from fat. The diets were made isocaloric by the addition of cellulose. Nutritional composition of the diet is shown in Table 1. The diets were fed ad libitum for 8 weeks to respective groups of animals. Body weights and food intake were measured three times per week. 
 
 Table 1: Nutritional content of the HFD-C and HFD-I diets. Full table Figures/tables index 
 
 Determination of acetate concentrations in serum and faeces 
 
 SCFAs were determined by gas chromatography in the colonic contents and serum of mice that where freshly culled. The method used was adapted from Richardson et al.35 Briefly, caecal contents were weighed (20–220 μg) and combined with 550 μl of PBS. Samples were vortex mixed for 1 min, centrifuged at 3,000 g for 10 min and the supernatant was collected. To 500 μl supernatant, 25 μl of internal standard and 2-ethylbutyric acid was added to give a final concentration of 5 mmol l−1. Acids were extracted by the addition of 250 μl concentrated hydrochloric acid and 1 ml diethyl ether followed by vortex mixing for 1 min. Samples were centrifuged for 10 min at 3,000 g and the ether layer was removed and transferred to a separate capped vial. N-methyl-N-t-butyldimethylsilyltrifluoroacetamide (MTBSTFA; Sigma) was added (100 μl) before heating at 80 °C for 20 min. 
 
 Gas chromatography was performed on a Hewlett Packard 5890 Series II instrument equipped with a flame ionization detector, split/splitless injector and a 10-m, 0.18 mm ID and 0.20 μm df Rtx-1 (Crossbond 100% dimethyl polysiloxane, Thames Restek UK, Ltd) capillary column. Injector and detector temperatures were 275 oC with the column temperature programmed from 63 °C for 3 min to 190 oC at 10 °C per min. Helium served as the carrier gas (head pressure 135 kPa) and injections (1 μl) were made in the split mode (50:1 split). Peak areas were recorded and all subsequent data manipulation was completed using ChemStation Software (Agilent Technologies, USA). External standards for acetate, propionate, n-butyrate, iso-butyrate, n-valerate and caproate were prepared at concentrations of 25, 12.5, 6.25, 1.25 and 0.625 mM and ethyl butyric acid was used as the internal standard at a concentration of 100 mM. Reported values were normalized according to the weight of original sample used. 
 
 Serum SCFA measurement 
 
 A 100–500-μl aliquot of serum was filtered through a 30-kDa micropartition system (Vivaspin RC VS02H22 filters, Sartorius Inc., Mississauga, ON, Canada) by centrifugation at 14,000 g at 4 °C for 90 min. An internal standard solution (25 μl) consisting of 100 mM ethylbutyrate and 100 mM formic acid was added to 225 μl of the protein-free filtrate supernatant in a 2-ml Hichrom vial (Agilent Technologies, South Queensferry, UK). To measure SCFA, 1 μl of each sample was injected into a 5,890 Series II GC system (HP, Crawley, UK) fitted with a NukolTM Capilllary Column (30 m × 0.53 mm × 1.0 μm, SUPELCOTM Analytical, UK) and flame ionization detector. The carrier gas, helium, was delivered at a flow rate of 14 ml min−1. The head pressure was set at 10 p.s.i. with split injection. Run conditions were: initial temperature 60 °C, 1 min; +20 °C min−1 to 145 °C; +4 °C min−1 to 200 °C, hold 25 min. Peaks were integrated using Agilent ChemStation software (Agilent Technologies, Oxford, UK) and SCFA content quantified by single-point internal standard method. Peak identity and internal response factors were determined using a 1-mM calibration cocktail including acetate, propionate and butyrate. 
 
 PET-CT analysis of acetate biodistribution 
 
 Mice were fasted overnight. Animals received 11C-acetate (~20 MBq) at the beginning of PET scan either through i.v. tail vein (n=3) or colonically by using tubing placed 1 cm into the rectum (n=4). At the time of the scan, animals were anaesthetized with a 2–2% isofluorane–oxygen mix. After the animals were placed in the micro PET/CT scanner (PET/CT (Siemens), a CT scan without contrast was performed, followed by the PET scan and lastly followed by a CT scan where contrast Ultravist 370 (Bayer, AG, Germany) was infused. 
 
 During the scan, animals were maintained at 1–1% isofluorane–oxygen mix and body temperature of 37 °C. The CT had an X-ray source of 80 kVp and 500 μA with exposure time 200 ms and isotropic resolution of 103 μm. The scan consisted of three bed positions with a 20% overlap. The CT scan was used for anatomical data and attenuation correction purposes. The PET system consisted of 64 lutetium oxyothosilicate based detectors blocks arranged in four contiguous rings, with a crystal ring diameter of 16.1 cm and an axial extent of 12.7 cm. Each detector block was composed of a 20 × 20 array of lutetium oxyothosilicate crystals coupled to a position sensitive photomultiplier tube via a light guide. Each crystal was 10 mm long and had a cross-sectional area of 1.51 × 1.51 mm. The crystal pitch was 1.59 mm in both axial and transverse directions. Inveon Research Workplace version 3 (Siemens) was used for data analysis. Images with matrix size 12 × 128, pixel size 0.776 mm2 and slice thickness 0.796 mm were reconstructed from the two-dimensional sinogram by two-dimensional-filtered backprojection using a ramp filter with a nyquist frequency of 0.5. Dynamic framing was used in reconstruction with 20 × 3 s frames, 8 × 30 s frames, 5 × 60 s frames and 10 × 300 s frames. Attenuation correction was also used to correct the image. Reconstructed PET images were then registered onto the CT images. PET signals on the desired region of interest were obtained over the scan period (1 h). Percentage injected dose (% ID per g) was calculated by using the following Equations (1) and (2), where; λ=0.693/T 1/2 , T 1/2 is the half-life of the radionuclide, I t is activity at a given time where I 0 is the starting activity and t is the time passed, C PET is the contrast of the image and ID is the activity of the injected acetate. 
 
 Effect of i.p. acetate on energy intake 
 
 Mice were fasted overnight before receiving either 500 mg kg−1 sodium acetate dissolved in 0.9% saline (n=22) or vehicle control (0.9% saline; n=21) pH 7.0, This dosage of acetate was similar to that used to suppress lipolysis in previous studies and was shown to be well tolerated14. Food intake was measured 1, 2, and 4 h post injection. 
 
 Effect of i.c.v. acetate on energy intake 
 
 Male Wistar rats 190–240 g (specific pathogen free; Charles River) were placed in a stereotaxic frame (David Kopf Instruments) under 0.5-2.5% isoflurane anaesthesia. A hole was drilled using a stereotactically mounted electric drill using coordinates calculated from the Rat Brain Atlas as described previously36, according to the coordinates of Paxinos and Watson37 (0.8 mm posterior to the Bregma in the midline and 6.5 mm below the surface of the skull). A permanent 22-gauge stainless steel cannula (Plastics One Inc., Roanoke, Virginia, USA) projecting to the third cerebral ventricle was implanted. Dental cement was used to hold the cannula in position anchored by three stainless steel screws inserted into the skull. The skin was approximated using nylon sutures. After a 7 day recovery period, animals were handled daily and acclimatized to the injection procedure. To ensure that cannulae were correctly positioned, rats received i.c.v. 150 ng angiotensin II in a 5-μl volume via a 28-gauge stainless steel injector placed into and projecting 1 mm below the tip of the cannula. Rats were observed for a prompt drinking response. A total volume of 5 μl was injected over 1 min to conscious, freely moving rats. For feeding studies, rats (n=15) were fasted overnight and then injected between 09:00 and 10:00 hours with sodium acetate (2.5 μmol) or an equivalent osmotic sodium chloride control (5 μl) and returned to their home cage. Food intake was measured at 1, 2 and 4 h post injection. After a 72-h washout period, rats received either the acetate or sodium chloride in a cross-over manner and food intake measured as previously described. 
 
 Effect of liposome encapsulate acetate on food intake 
 
 Nanoparticle design was based upon our previous studies where PEGylated liposomes were formulated for labelling and visualization of cells38, or specifically designed for preferential uptake in xenograft tumours15. Liposomes were prepared by the thin-film hydration method39. Liposomes were prepared with either acetate (1 M, pH 2.3) to form liposome-encapsulated acetate (LITA) nanoparticles or HEPES for use as a control. Particle size was determined using a Malvern Zetasizer (Malvern Instruments, UK). Quantification of acetate encapsulated within LITA nanoparticles was determined using 1H nuclear magnetic resonance (NMR) spectroscopy. LITA formulation (200 μl) was scanned with addition of albumin that binds to acetate in free solution reducing the NMR signal for the compound40. A liposome-free control solution containing an equivalent concentration of acetate (4 mM) was also scanned with and without the addition of albumin (2 g). LITA solution was scanned following the addition of lactate (5.2 mg sodium lactate) to act as a quantitative control. Spectra were obtained using a Bruker DRX 11.74T NMR spectrometer. Spectra were analysed using MestRe-C NMR spectroscopy software (Santiago de Compostela, Spain). 
 
 To assess short-term biodistribution, a liposome formulation containing an additional 0.1% of a rhodamine–lipid complex (DOPE-Rhodamine: 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-(lissamine rhodamine B sulfonyl) was used to determine biodistibution through ex vivo histological analysis. Samples were collected 4 h post i.p. injection (n=4). No significant accumulation of liposome was observed in the brain of the treated mice despite being present in the liver and heart. 
 
 The effect of acetate on behaviour 
 
 Mice were fasted overnight before receiving either a single i.p. injection of saline, 500 mg kg−1 acetate or 2.5 M LiCl as a positive control for aversive behaviour41 (n=8 per group). The behavioural patterns of each mouse were observed for 15 s every 5 min from the time of injection until 1 h post injection. Behaviours was classified using a modified version of a previously published protocol42. Briefly, behaviours was classified into 10 different categories: feeding, drinking, locomotion (including rearing and climbing), bed making, burrowing, grooming, still, sleeping, head down (animal in abnormal body posture: back hunched, eyes shut or half-shut and pilo erect—indicative of impaired health status) and tremors. 
 
 Acetate tolerance test 
 
 Glucose levels were determined from blood taken from mouse tails using a Glucometer Elite glucometer (Bayer Corp.). Experiments were performed on ad libitum fed mice at 14:00 h as previously described for insulin tolerance tests18 but instead of insulin, animals were injected i.p. with either 500 mg kg−1 sodium acetate or saline control (n=9–10). Blood glucose values were then determined at the times indicated. Results were expressed as fold change of initial blood glucose concentration before injections. 
 
 Plasma PYY and GLP-1 hormone analysis 
 
 All samples were assayed in duplicate and in a single assay to eliminate inter assay variation. Plasma PYY and GLP-1 were assessed using an established in-house radioimmunoassay as described previously43, 44. 
 
 Hypothalamic quantitative PCR 
 
 This was carried out using the methods described by Bewick et al.45 Quantitative reverse transcriptase PCR (RT-qPCR) was used to study the expression of the different target genes. Total RNA was extracted from the whole hypothalami using TRIZOL (Invitrogen) according to the manufacturer’s protocol. All samples were treated by DNaseI (Invitrogen) before the reverse transcription. First-strand cDNAs were prepared using 1 μg RNA and SuperScriptII Reverse Transcriptase (Invitrogen) in the presence of random hexamer and oligo(dT) primers (Promega, Charbonnières-les-Bains, France). The qPCRs were performed using the Light Cycler Fast Start DNA Master SyBR Green I kit (Roche, Meylan, France) in the presence of specific primer pairs that were selected to amplify small fragments (100–200 bp). PCR products were checked for specificity by measuring their melting temperature. Samples (in duplicate) were quantified by comparison with a standard curve obtained by dilutions of purified-specific cDNAs. 
 
 Measurements of AGRP and POMC mRNA expression 
 
 RNA was extracted from dissected hypothalamus using Absolutely RNA microprep kit from Stratagene (La Jolla, CA, USA). The gene transcription for AgRP and POMC in the ARC of the hypothalamus was determined using real-time RT-PCR, and results were expressed as a ratio to the expression of the constitutive gene cyclophilin. The sequences of TaqMan probes and primers for cyclophilin (GenBank accession no. M15933) were: forward primer 5′-CCCACCGTGTTCTTCGACAT; reverse primer 5′-TGCAAACAGCTCGAAGCAGA-3′; and probe 5′-CAAGGGCTCGCCATCAGCCG-3′. For AGRP, they were: forward primer 5′-TTGGCAGAGGTGCTAGATCCA-3′; reverse primer 5′-AGGACTCGTGCAGCCTTACAC-3′; and probe 5′-CGAGTCTCGTTCTCCGCGTCGC-3′. The probe and primers for POMC (assay identification no. Rn00595020_ml) were purchased from Applied Biosystems. 
 
 Manganese-enhanced MRI 
 
 MEMRI was performed using a 9.4-Tesla Varian INOVA imaging system (Varian Inc., USA) as described previously46. A fast spin-echo multi-slice sequence was applied with the following parameters: TR= 600 ms, TE=10 ms, matrix size= 256 × 192, FOV=25 × 25 mm and average=1 acquiring 46 × 0.4 mm thick slices. An array of 66 acquisitions was set up so that the 46 slices were acquired 66 times throughout the infusion. Normalized percentage enhancement in signal intensity was calculated for the ARC, VMH, PVN, periventricular nucleus (PE) and the nucleus of tractus solitarius27, 43. 
 
 Hypothalamic measurement of AMP kinase 
 
 Animals were killed by decapitation, brains were immediately dissected and the hypothalamus was removed and snap-frozen in liquid nitrogen. Frozen tissues (~100 mg) were homogenized in 0.4 ml of ice-cold 50 mm HEPES, pH 7.4, 50 mm sodium fluoride, 5 mm sodium pyrophosphate, 250 mm sucrose, 1 mm EDTA, 1 mm dithiothreitol, 1 mm benzamidine, 1 mm trypsin inhibitor, 0.1% (w/v) phenylmethylsulfonyl fluoride using an UltraTurax homogenizer (3 × 30-s bursts). Insoluble material was removed by centrifugation and the resulting supernatant was used for immunoprecipitation of AMPK and western blot analysis. 
 
 Immunoblotting and antibodies 
 
 Samples were boiled in electrophoresis sample buffer and resolved on polyacrylamide gels. Proteins were transferred into PVDF membrane (Immobilon-FL, Millipore) and blocked with PBS containing 5% skimmed milk powder for 1 h. Antibodies were diluted in 5 ml high salt Tween buffer (20 mM Tris, pH 7.4, 500 mM NaCl and 0.5% Tween (v/v)), and incubated with the membrane. Primary antibodies used for immunoblotting are as follows: anti-AMPK-β1/2 (in-house) (dilutions 1:3,000–1:10,000 for blotting), anti-phospho-ACC (S79) (Cell Signalling, cat. no. 3661), anti-phospho-AMPK (PT172) (Cell Signalling, cat. no. 2535) anti-β-actin (Sigma, cat. no. A5316). 
 
 Primary antibodies were detected using fluorescently linked secondary antibodies (Alexa Fluor, Invitrogen, goat anti rabbit: A21109 and goat anti mouse: A21058). These were visualized using an Odyssey infrared imager (Li-Cor Biosciences). Quantification of results was performed using Odyssey software and expressed as a ratio of the signal obtained with the phospho-specific antibody relative to the appropriate total antibody. Full-length images of cut immunoblots are shown in Supplementary Fig. 1. 
 
 The effect of acetate on hypothalamic metabolism 
 
 [2-13C] acetate (500 mg kg−1) or [U-13C] inulin (100 mg) were administrated to 8–10-week-old C57BL/6J male mice (Charles River, Spain) after an overnight fasting (16 h) either with i.p. (n=18) or by gavage (n=4), respectively. All mice were anaesthetized with 4% isoflurane (3 l per min, 99% oxygen), and cerebral metabolism was arrested within 1.5 s using a high-power (5 kW) microwave fixation system (TMW-6402C, Muromachi Kikai Co. Ltd, Tokyo, Japan) immediately (0 min), 15 and 30 min after acetate, or 180 min after inulin, administrations. Fixed brains were dissected and hypothalamus and remaining brain biopsies were obtained and maintained frozen (−80 °C) until HR-MAS analyses. 13C (125,03 MHz) and 1H HR-MAS (500,13 MHz) spectra were acquired at 11.7 T (4 °C, 4,000 Hz rotation) with a Bruker AVANCE wide bore spectrometer equipped with a MAS accessory (Bruker Biospin, Rheinstetten, Germany). 1H-decoupled 13C HR-MAS spectra were acquired using a pulse-acquire sequence, with WALTZ-16 1H decoupling applied during the acquisition and relaxation delay periods. Conditions were π/4 pulses, 8,192 or 16,384 scans (for [2-13C] acetate or [U-13C] inulin measurements, respectively), 64 k data points, 5 s recycle delay. The 13C spectra were processed with Mestrelab ( http://mestrelab.com/). Chemical shifts of the 13C resonances were referred to the acetate C2 resonance (24.5 p.p.m.), and the 13C incorporation was normalized to the myo-inositol C1+C3 resonance (73.2 p.p.m.), which provides a useful internal reference from which all 13C resonances can be normalized independently of the amount of tissue20, 47, introducing appropriate corrections for nuclear Overhausser enhancement and saturation. 
 
 1H HR-MAS spectra from the same biopsies used for 13C HR-MAS acquisitions were acquired using the Carr-Purcell-Meiboom-Gil sequence. Acquisition parameters were 5 s water pre-saturation, echo time=144 ms, t=1 ms, n=100, 10 kHz spectral width, 32 k data points and 256 scans. Metabolite concentrations were evaluated using a modified version of the LCModel processing software (Linear Combination of Model Spectra, http://s-provencher.com/pages/schtm)48. 
 
 Statistical tests were performed using two-tailed unpaired Student’s t-test between values in the different time points or areas. Observations that fell below the Q1-1.5 × IQR (interquartile range) or above the Q3+1.5 × IQR range (with Q 1 and Q 3 representing the upper and lower quartiles values and IQR, the difference between Q 3 and Q 1 ) were considered outliers and were not taken into account for statistical evaluations. 
 
 Data analysis 
 
 Analyses were performed using Graph Pad Prism (GraphPad Software, San Diego, CA, USA) or Stata (StataCorp LP, College Station, TX, USA). All data was tested for normality using Shapiro–Wilk test. Non-normally distributed data was log transformed to normalize the distribution. Comparison between groups was carried out by two-sided unpaired Student’s t-test for two groups and one-way analysis of variance (ANOVA) with post hoc Tukey or Bonferroni correction if there were more than two groups. I.c.v. cross-over acetate injection studies were compared using a two-sided paired Student’s t-test. Given the cumulative nature of both MEMRI and PET signal intensity data, differences in signal intensity profile between the regions of interest in all experimental groups were analysed using GEE and the Mann–Whitney U-test with commercial statistical software (Stata, version 9.1; StataCorp), which compare profiles for the entirety scan. All results and graphs are expressed as means±s.e.m. Results were considered statistically significant when P<0.05, with the significance level indicated as *P<0.05, **P<0.01 and ***P<0.001 ||||| Peter Cade/Getty 
 
 A study of mouse metabolism suggests that a product of fibre fermentation may be directly affecting the hypothalamus, a region of the brain involved in regulating appetite. 
 
 People have long been told that a diet high in fibre can help to fight obesity, but how it does so has been unclear. “There has been lots of epidemiological information showing a relationship between fibre and obesity, but no one has been able to connect the epidemiological results with actual mechanisms,” says Jimmy Bell, a biochemist at Imperial College London who worked on the research, published today in Nature Communications1. 
 
 Until now, a high-fibre diet was thought to help keep weight down by stimulating the release of appetite-suppressing hormones in the gut2, says Bell, but humans do not seem to show the same increase in these hormones that mice do. 
 
 So Bell and his colleagues decided to look elsewhere. An obvious candidate, they thought, might be one of the products of fibre fermentation in the gut. In particular they focused on the short-chain fatty acid acetate, because it is the most abundant and is known to circulate throughout the bloodstream. 
 
 They fed mice fibre labelled with carbon-13, which has an additional neutron from the more common carbon-12 that gives its nuclei a magnetic spin and therefore makes it easy to track as it progresses through the body's chemical reactions. The fibre was fermented as usual into acetate, which turned up not only in the gut, but also in the hypothalamus, a part of the brain known to be involved in regulating appetite. There, the researchers found, it was metabolized through the glutamine-glutamate cycle, which is involved in controlling the release of neurotransmitters associated with appetite control. The same model has been proposed for acetate metabolism after drinking alcohol. 
 
 The mice fed with large doses of fermentable fibre ate less food, and ended up weighing less than control mice that were fed unfermentable fibre. 
 
 'Simplistic' approach 
 
 William Colmers, an electrophysiologist who studies the effect of neurotransmitters in the hypothalamus at the University of Alberta in Edmonton, Canada, says he thinks that the experimental work is solid, but worries that the results have been over-interpreted. “Much of it is extremely speculative,” he says. For one thing, the dietary fibre levels were around 11%. At that level, “the room would be full of mouse farts”, he says, so the animals may simply have been eating less because they were uncomfortable. 
 
 Colmers adds that the hypothesis of how acetate in the hypothalamus was affecting the release of neurotransmitters to decrease appetite is “a simplistic view of how the nervous system works”. The release of neurotransmitters is “excruciatingly well regulated”, he says, and not as sensitive to manipulation by changes in biochemistry as the authors suggest. 
 
 Although the work was done in mice, Bell says that he sees “no reason” why the same mechanism shouldn’t be at work in humans. “Acetate is known to be metabolized in the human brain, and we have the right microbiota in our gut for the fermentation of fibre,” he says. 
 
 Bell and his colleagues are preparing to test their ideas in people. The question, however, is how much fibre do you have to eat? Most people's diet contains between 10 and 20 grams of fibre a day, and it can be difficult to increase this amount substantially. So Bell and his colleagues are working with companies that are looking into enriching fibre with acetate to boost the digestive system, and into ways of encasing acetate in nanoparticles so that it releases slowly throughout the day to help control appetite. “It’s sort of a way of having your cake, and not eating it,” says Bell. ||||| A pill that switches off hunger is on the horizon after scientists discovered an ‘anti-appetite’ molecule which tells the body to stop eating. 
 
 Researchers at Imperial College discovered that people feel full when eating fruit and vegetables because fibre releases acetate into the gut. 
 
 They believe that a pill derived from acetate could be created to help people cut down on food without experiencing any cravings. 
 
 One in four adults in England is obese and that figure is set to climb to 60 per cent of men and 50 per cent of women by 2050. 
 
 Obesity and diabetes already costs the UK over £5billion every year which is likely to rise to £50 billion in the next 36 years. 
 
 Large amounts of acetate are released when plants and vegetables are digested by bacteria in the colon. The scientists tracked the molecule and found that it eventually ended up in the hypothalamus region of the brain, which controls hunger. 
 
 The new study suggests obesity has become an epidemic because we have replaced the healthy diet of the past with processed food, which does not react with gut bacteria to produce acetate. So the brain does not receive a signal telling it to stop eating. 
 
 The average diet in Europe today contains about 15 g of fibre per day. In Stone Age times it was around 100g per day. 
 
 "Unfortunately our digestive system has not yet evolved to deal with this modern diet and this mismatch contributes to the current obesity epidemic,” said Professor Gary Frost, of Imperial College. 
 
 Although scientists say their research should encourage more people to eat more fruit and vegetables, they also believe it could pave the way for new drugs to help dieters. 
 
 Prof Frost added: "Our research has shown the release of acetate is central to how fibre suppresses our appetite and this could help scientists tackle overeating. 
 
 "The major challenge is to develop an approach that will deliver the amount of acetate needed to suppress appetite but in a form that is acceptable and safe for humans. 
 
 "Developing these approaches will be difficult but it is a good challenge to have and we are looking forward to researching possible ways of using acetate to address health issues around weight gain.” 
 
 The study analysed the effects of a form of dietary fibre called inulin which comes from chicory and sugar beets and is also added to cereal bars. 
 
 Experiments on mice found those fed on a high fat diet with added inulin ate less and gained less weight than animals given a lot of fat diet with no inulin. 
 
 They also noticed that the acetate acculmulates in the hypothalamus of the brain where it triggers a series of chemical events which fire neurons and suppress hunger. 
 
 The research also showed when acetate was injected into the bloodstream, the colon or the brain it reduced the amount of food eaten by the mice. 
 
 Prof Jimmy Bell, of the Medical Research Council, Cambridge, who collaborated in the research, said: "It is exciting we have started to really understand what lies behind fibre's natural ability to suppress our appetite and identified acetate as essential to the process. 
 
 "In the context of the growing rates of obesity in western countries, the findings of the research could inform potential methods to prevent weight gain." 
 
 Acetate is only active for a short amount of time in the body so an ‘acetate pill’ would need to be able to mimic the chemical’s slow release into the gut. 
 
 Prof David Lomas, chair of the MRC's population and systems medicine board, said it is becoming increasingly clear the interaction between the gut and the brain plays a key role in controlling how much food we eat. 
 
 He added: "Being able to influence this relationship, for example using acetate to suppress appetite, may in future lead to new, non surgical treatments for obesity." ||||| TIME Health For more, visit TIME Health 
 
 Scientists have figured out the reason fiber is such a wonder food: It contains an anti-appetite molecule called acetate. 
 
 Acetate, the researchers discovered, is naturally released when fiber is digested in the gut, and when it’s released, it is taken to the brain where it signals us to stop eating. 
 
 Fiber has long been known to satiate appetite and keep us full for longer, but previous research supposed the reason was that it takes longer to digest, keeping us satisfied for longer after we’ve stopped eating. But this new research published in the journal Nature Communications shows that the acetate released when we digest roughage lowers our appetites when it gets directly into our bloodstream, colon or brain. 
 
 The researchers looked at a dietary fiber called inulin, which comes from chicory and sugar beets, and is often present in cereal bars. They fed mice a diet high in fat with additional inulin. These mice ate less and gained less weight than mice who did not consume inulin, and when the scientists took a deeper look, they discovered that the inulin-eating mice had higher levels of acetate in their gut. So, they used PET scans to track the inulin through the mice. 
 
 They discovered that the acetate traveled from the colon to the liver and heart, and finally made it to the the area of the brain that deals with hunger, the hypothalamus region. Using more imaging, they determined that the acetate accumulates and spurs chemical reactions in the brain that send signals that suppress hunger. 
 
 Eating more fiber, found in foods like nuts, oatmeal, beans, lentils, apples and blueberries, is one of the better ways to feel full and satisfied, and can help with weight management. Science says so.
– Experts have long suggested that fiber keeps us feeling full because it takes a long time to digest, but new research challenges that notion—and may point the way to a new anti-hunger pill. The key is a short-chain fatty acid called acetate, which emerges as fiber is digested. Acetate then makes its way to the brain's hypothalamus, where it builds up and triggers chemical reactions that tell us we're full, Time reports. Researchers reached this conclusion by scanning the progress of a dietary fiber called inulin through the bodies of mice. Those mice who ate fatty diets rich in inulin gained less weight than mice who didn't eat inulin. But one electrophysiologist not related to the study points out that the mice were fed dietary fiber levels of about 11%. He tells Nature that at such a level, "the room would be full of mouse farts"—and perhaps the mice were eating less because they felt gassy. The researchers plan to next test the idea in humans. So could we eventually see an acetate-based diet pill? It's possible, the Telegraph suggests: "The major challenge is to develop an approach that will deliver the amount of acetate needed to suppress appetite but in a form that is acceptable and safe for humans," a researcher says.