Switching from Sugar- to Artificially-Sweetened Beverages: A 12-Week Trial.

BACKGROUND: Consumption of sugar-sweetened beverages (SSBs) forms the primary source of added sugar intake and can increase the risk of metabolic disease. Evidence from studies in humans and rodents also indicates that consumption of SSBs can impair performance on cognitive tests, but that removing SSB access can ameliorate these effects. METHODS: The present study used an unblinded 3-group parallel design to assess the effects of a 12-week intervention in which young healthy adults (mean age = 22.85, SD = 3.89; mean BMI: 23.2, SD = 3.6) who regularly consumed SSBs were instructed to replace SSB intake with artificially-sweetened beverages (n = 28) or water (n = 25), or (c) to continue SSB intake (n = 27). RESULTS: No significant group differences were observed in short-term verbal memory on the Logical Memory test or the ratio of waist circumference to height (primary outcomes), nor in secondary measures of effect, impulsivity, adiposity, or glucose tolerance. One notable change was a significant reduction in liking for strong sucrose solutions in participants who switched to water. Switching from SSBs to 'diet' drinks or water had no detectable impact on cognitive or metabolic health over the relatively short time frame studied here. This study was prospectively registered with the Australian New Zealand Clinical Trials Registry (ACTRN12615001004550; Universal Trial Number: U1111-1170-4543).

Comparable metabolic effects of isocaloric sucrose and glucose solutions in rats.

Much of the global increase in sugar intake is attributable to rising consumption of sugar-sweetened beverages (SSBs). Because people compensate poorly for liquid calories, SSB consumption increases total energy intake, raising the risk of harmful metabolic effects in addition to possible effects of sugars per se. Glucose and fructose, the constituent sugars in sucrose, can exert distinct effects on metabolism and also differ in their satiating properties, suggesting that compensation for the calories in these sugars may also vary. In light of claims that the fructose within sucrose is particularly harmful, the present study compared the effects of giving rats access to either a sucrose or an isoenergetic glucose solution. Adult male rats were fed standard chow and water supplemented with 95 ml of 10% glucose (Glucose group; n = 10), 9% sucrose solution (Sucrose group; n = 10) or water only (Control group; n = 10) daily for 7 weeks. Sugar-fed groups had higher total energy intakes than the Control group, but the extent of this incomplete compensation did not vary between Sucrose and Glucose groups. In a short-term compensation test, sugar groups were less sensitive to the effects of a sweet pre-meal, with no differences between the Glucose and Sucrose groups. Relative to water, both sugars reduced insulin sensitivity after 4 weeks on the diets and elevated fat mass at 7 weeks. Results suggest that sucrose and glucose induce comparable metabolic impairments and alter the homeostatic regulation of food intake even under conditions where daily access is capped.

Metabolic and cognitive improvement from switching to saccharin or water following chronic consumption by female rats of 10% sucrose solution.

High consumption of sugar-sweetened beverages (SSBs) is a risk factor for weight gain and metabolic disease. Whether this risk is reduced by switching to 'diet' beverages containing low-calorie sweeteners (LCS) is controversial. Two experiments modeled whether a switch from SSB to LCS beverages produced positive outcomes on behavioral and metabolic measures. Both experiments consisted of a Stage 1, in which adult female rats received unrestricted access to 10% sucrose solution in addition to chow and water for 4 (Experiment 1) or 8 weeks (Experiment 2). In Stage 2 rats were switched to either saccharin (Suc-Sacch) or water (Suc-Water) or remained on 10% sucrose (Suc-Suc) for a further 4 (Experiment 1) or 7 weeks (Experiment 2). Experiment 2 contained a fourth group that was maintained on water throughout (Water-Water). In both experiments energy intake and weight gain in Stage 2 was reduced for Suc-Sacch and Suc-Water groups relative to the Suc-Suc groups and at cull the Suc-Suc groups showed poorer insulin sensitivity and greater g/kg fat than Suc-Water and Suc-Sacch groups. In Experiment 2 short-term place recognition memory was impaired at the end of Stage 1 but recovered to a similar extent in the Suc-Water and Suc-Sacch groups; when the latter groups were compared with the Water-Water group, recovery was found to be essentially complete. A higher saccharin concentration in Experiment 2 than in Experiment 1 increased absolute amounts of saccharin ingested but intake solution volumes remained low. These results show that switching from sucrose to either water or saccharin produces equivalent improvements on both metabolic and cognitive measures.

Alternating or continuous exposure to cafeteria diet leads to similar shifts in gut microbiota compared to chow diet.

SCOPE: Overconsumption of energy-rich food is a major contributor to the obesity epidemic. The eating habits of many people are characterized by the cycling between overconsumption of energy-rich foods and dieting, the effects of which on the microbiota are currently unknown. METHODS AND RESULTS: We compared the fecal microbiota of rats either continuously fed chow or palatable cafeteria diet to a "cycled" group switched between the two diets (chow for 4, cafeteria for 3 days/wk, n = 12/group) over 16 wk. Enriched bacterial metabolic pathways were predicted, and a range of metabolic parameters was correlated to microbial taxa and pathways. Cycled rats showed large excursions in food intake on each diet switch. When switched from chow to cafeteria, they overconsumed, and when switched back to chow they underconsumed relative to those maintained on the two diets. Metabolic parameters of cycled rats were intermediate between those of the other diet groups (p < 0.05). The microbiota of cycled rats was nearly indistinguishable from rats under constant cafeteria diet, and both groups were significantly different to the chow group. Correlation analyses identified microbial metabolic pathways associated with an obese phenotype. CONCLUSION: These data suggest that continuous or intermittent exposure to palatable foods have similar effects on the gut microbiota.

Individual differences in saccharin acceptance predict rats' food intake.

Following previous results indicating that low acceptance of saccharin-sweetened yoghurt was associated with slower weight gain, the aim of this experiment was to determine which of three measures of individual differences would predict subsequent chow consumption, body weight gain, and fat mass. Pre-test measures consisted of amount of running in an activity wheel, amount of 0.1% saccharin solution consumed over 24h, and performance on an elevated plus maze (EPM). Rats were then maintained for three weeks on a diet of standard chow and water. Subsequent post-testing repeated the procedures used in pre-testing. The rats were then culled and fat pads excised and weighed. Pre-testing revealed a negative correlation between saccharin acceptance and activity, while neither measure correlated with anxiety in the EPM. Pre-test saccharin acceptance was positively correlated with subsequent chow consumption, percent weight gain, and g/kg fat mass. Multiple regression analyses including all three pre-test measures confirmed saccharin acceptance as a predictor of chow consumption and, marginally, of fat pad mass, while high anxiety predicted low percent body weight gain.

Sweetening yoghurt with glucose, but not with saccharin, promotes weight gain and increased fat pad mass in rats.

The claim that non-nutritive sweeteners accelerate body weight gain by disrupting sweet-calorie associations was tested in two experiments using rats. The experiments were modelled on a key study from a series of experiments reporting greater body weight gain in rats fed yoghurt sweetened with saccharin than with glucose (Swithers & Davidson, 2008). Both of the current experiments likewise compared groups fed saccharin- or glucose-sweetened yoghurt in addition to chow and water, while Experiment 1 included a third group (Control) given unsweetened yoghurt. In Experiment 1, but not in Experiment 2, rats were initially exposed to both saccharin- and glucose-sweetened yoghurts to assess their relative palatability. We also tested whether the provision of an energy-dense sweet biscuit would augment any effects of saccharin on food intake and weight gain, as seemingly predicted by Swithers and Davidson (2008). In Experiment 1 there were no differences in body weight gain or fat pad mass between the Saccharin and Control group, whereas the Glucose group was the heaviest by the final 5 weeks and at cull had the largest fat pads. Greater acceptance of saccharin predicted more weight gain over the whole experiment. Consistent with past reports, fasting blood glucose and insulin measures did not differ between the Saccharin and Control groups, but suggested some impairment of insulin sensitivity in the Glucose group. Experiment 2 found similar effects of glucose on fat mass, but not on body weight gain. In summary, adding saccharin had no detectable effects on body-weight regulation, whereas the effects of glucose on fat pad mass were consistent with previous studies reporting more harmful effects of sugars compared to non-nutritive sweeteners.

Effects of long-term cycling between palatable cafeteria diet and regular chow on intake, eating patterns, and response to saccharin and sucrose.

When exposed to a diet containing foods that are rich in fat and sugar, rats eat to excess and gain weight. We examined the effects of alternating this diet with laboratory chow on intake of each type of diet, the eating elicited by a palatable food (biscuits), and the drinking elicited by sweet solutions that did (sucrose) or did not (saccharin) contain calories. Each week for 13 weeks, cycled rats were provided with the cafeteria diet for three successive days/nights and the chow diet for the remaining four days/nights, whereas other rats received continuous access to either the cafeteria or the chow diets. On each of the 13 weeks, cycled rats ate more across the first 24 hour exposure to the cafeteria diet than rats continuously fed this diet. In contrast, cycled rats ate less across the first 24 hour exposure to the chow diet than rats continuously fed this diet and ate less when presented a novel palatable biscuit than chow-fed rats. The three groups exhibited similar licks per cluster to saccharin, but cafeteria-fed and cycled rats showed fewer clusters than chow-fed rats. In contrast, chow-fed rats and cycled rats exhibited more licks per cluster to sucrose than cafeteria-fed rats, but all three groups had a similar number of clusters. The results were discussed in relation to the effects of diet cycling on eating patterns, body weight, and 'wanting' and 'liking'. These findings with rats may have important implications for yo-yo dieting in people.

Rats eat a cafeteria-style diet to excess but eat smaller amounts and less frequently when tested with chow.

BACKGROUND: Obesity is associated with excessive consumption of palatable, energy dense foods. The present study used an animal model to examine feeding patterns during exposure to and withdrawal from these foods. METHODS: Male Sprague Dawley rats were exposed to standard lab chow only (Chow rats) or a range of cafeteria-style foods eaten by people (Caf rats). After 1, 4, 7 and 10 weeks of diet in their home cage, rats were subjected to 24-hour test sessions in a Comprehensive Lab Animal Monitoring System (CLAMS). In the first two test sessions, Chow rats were exposed to standard lab chow only while Caf rats were exposed to a biscuit and high-fat chow diet. In the final two test sessions, half the rats in each group were switched to the opposing diet. In each session we recorded numbers of bouts, energy consumed per bout, and intervals between bouts across the entire 24 hours. RESULTS: Relative to Chow rats, Caf rats initiated fewer bouts but consumed more energy per bout; however, their motivation to feed in the CLAMS declined over time, which was attributed to reduced variety of foods relative to their home cage diet. This decline in motivation was especially pronounced among Caf rats switched from the palatable CLAMS diet to standard lab chow only: the reduced energy intake in this group was due to a modest decline in bout frequency and a dramatic decline in bout size. CONCLUSIONS: Exposure to a cafeteria-diet, rich in variety, altered feeding patterns, reduced rats' motivation to consume palatable foods in the absence of variety, and further diminished motivation to feed when palatable foods were withdrawn and replaced with chow. Hence, variety is a key factor in driving excessive consumption of energy dense foods, and therefore, excessive weight gain.

Extended exposure to a palatable cafeteria diet alters gene expression in brain regions implicated in reward, and withdrawal from this diet alters gene expression in brain regions associated with stress.

Like people, rodents exposed to energy-rich foods over-eat and become overweight. Removal of this diet activates stress systems, which may explain why people have difficulty dieting. We exposed rats to energy-rich foods in order to identify changes in the brain induced by that diet and by its removal. Sprague Dawley rats were fed lab-chow or an energy-rich cafeteria diet (plus chow). Following 6 or 15 weeks, half of each group was switched to the opposing diet. Rats were culled 48-h later. We measured fat mass, plasma hormones, and assessed brains for mRNA expression of several genes. Cafeteria-fed rats consumed more kilojoules, weighed more and had elevated leptin (plus reduced CORT at 15 weeks) relative to chow-fed rats. Fifteen weeks of cafeteria diet suppressed µ-opioid and CB1 receptor mRNA in the VTA, but elevated amygdala GR, and 6 weeks of cafeteria diet reduced BDNF, compared to chow-fed rats. Rats switched to the cafeteria diet ate similar amounts as rats maintained on the diet, and switching to cafeteria diet after 15 weeks reduced amygdala GR expression. Rats switched to chow ate less than rats maintained on chow, and switching to chow following 15 weeks of cafeteria diet increased hypothalamic CRH mRNA. Therefore, 15 weeks of cafeteria diet produced changes in brain regions implicated in reward processes. Switching these rats to chow activated the HPA axis, while switching chow-fed rats to the cafeteria diet decreased GR expression in the amygdala, a region associated with stress. These findings have implications for dieting in humans.

Altered feeding patterns in rats exposed to a palatable cafeteria diet: increased snacking and its implications for development of obesity.

BACKGROUND: Rats prefer energy-rich foods over chow and eat them to excess. The pattern of eating elicited by this diet is unknown. We used the behavioral satiety sequence to classify an eating bout as a meal or snack and compared the eating patterns of rats fed an energy rich cafeteria diet or chow. METHODS: Eight week old male Sprague Dawley rats were exposed to lab chow or an energy-rich cafeteria diet (plus chow) for 16 weeks. After 5, 10 and 15 weeks, home-cage overnight feeding behavior was recorded. Eating followed by grooming then resting or sleeping was classified as a meal; whereas eating not followed by the full sequence was classified as a snack. Numbers of meals and snacks, their duration, and waiting times between feeding bouts were compared between the two conditions. RESULTS: Cafeteria-fed rats ate more protein, fat and carbohydrate, consistently ingesting double the energy of chow-fed rats, and were significantly heavier by week 4. Cafeteria-fed rats tended to take multiple snacks between meals and ate fewer meals than chow-fed rats. They also ate more snacks at 5 weeks, were less effective at compensating for snacking by reducing meals, and the number of snacks in the majority of the cafeteria-fed rats was positively related to terminal body weights. CONCLUSIONS: Exposure to a palatable diet had long-term effects on feeding patterns. Rats became overweight because they initially ate more frequently and ultimately ate more of foods with higher energy density. The early increased snacking in young cafeteria-fed rats may represent the establishment of eating habits that promote weight gain.

The effects of FG 7142 on sensory-specific satiety in rats.

Three experiments used intake, clusters, and licks per cluster to study the effects of the GABA inverse agonist, FG 7142, on sensory-specific satiety in rats. In Experiment 1, rats were offered one of two palatable solutions and 30min later tested with the same or the other solution. Rats that received the same solution consumed less, exhibited fewer clusters, fewer licks per cluster and a more rapid decline in rate of licking than rats tested with the other solution. In Experiments 2 and 3, rats tested with the same solution under FG 7142 showed fewer clusters and fewer licks per cluster than vehicle rats. Rats tested with the other solution under FG 7142 showed fewer licks per cluster but more clusters than vehicle rats. The results were discussed in terms of the distinction between "liking" and "wanting" and the role of GABA in the former but not the latter.