Sucrose Intake Research Articles

Sucrase isomaltase dysfunction reduces sucrose intake in mice and humans

Sucrase isomaltase dysfunction reduces sucrose intake in mice and humans

Metabolic management of a successful pregnancy and postpartum complications in fructose-1,6-bisphosphatase deficiency.

Fructose-1,6-bisphosphatase (FBPase) deficiency is a rare, inborn error of metabolism, that causes hypoglycemia and lactic acidosis in response to inadequate glucose intake and/or high intakes of fructose, sucrose, or sorbitol. Pregnancy in women with FBPase deficiency puts them at high risk for metabolic decompensation due to increased glucose demands from the growing fetus. Here we report a 31-year-old primipara who was treated starting at 14 weeks gestation with a diet high in complex carbohydrates and low in fructose, sucrose, and sorbitol and close monitoring of glucose levels throughout her pregnancy. She delivered a healthy 2860 g baby at 37 weeks via vaginal delivery with no complications or hypoglycemia. At 5 months postpartum and 5 months of life, the patient and baby are doing well, although the patient experienced an episode of hypoglycemia and lactic acidosis at 4 months postpartum due to the increased metabolic demands of breastfeeding. This report adds to the limited case reports that discuss outcomes and proposed interventions during pregnancy in individuals with FBPase deficiency.

The link between the risk of cardiovascular diseases and the intake of different types of dietary carbohydrates in Iranian adults.

The risk of cardiovascular diseases (CVDs) may be influenced by dietary carbohydrates. The aim of this study was to investigate the link between CVDs and the intake of carbohydrates. In this cross-sectional study, data was extracted from the Prospective Epidemiologic Research Studies in Iran (PERSIAN) cohort in Sabzevar, Iran. A total of 4241 adults, including 1535 patients with CVDs and 2706 people without CVDs, were included. A validated 237-item food frequency questionnaire was used to estimate the intake of different types of dietary carbohydrates. A positive association was found between stroke and dietary intake of starch (OR = 1.108; 95% CI, 1.005-1.220; P = 0.039). Additionally, a negative association was found between stroke and dietary intake of sucrose (OR = 0.97; 95%CI, 0.94-0.99; P = 0.037). No association was found between other types of CVDs and the intake of different types of carbohydrates. This study provided some evidence for the association between CVDs and different types of dietary carbohydrates. Consumption of starch may increase the risk of stroke, while a higher intake of sucrose may decrease the risk of stroke. Further studies are warranted.

Intriguing hepatoprotective effects of sucrose on hepatocellular carcinoma pathogenesis

Chronic liver disease is closely linked to dietary intake factors, such as high consumption of simple carbohydrates including sucrose. In this study, the influence of sucrose on the development of hepatocellular carcinoma (HCC), the most common primary liver malignancy, was explored. Using the hepatocarcinogen diethylnitrosamine (DEN) to induce HCC in the rat, we co-administered sucrose with DEN. The co-administration significantly modified body, liver and pancreas weight, as well as, serum fatty acids and triglycerides. DEN caused liver structural alteration, fibrosis, and tumor formation; surprisingly, co-administration with sucrose restored hepatic lipids, improved liver architecture, and reduced fibrosis and tumor development. Sucrose intake negatively regulated tumor markers and cell proliferation, and reduced the expression of genes associated with lipid metabolism and oxidative stress response. These findings highlight a hepatoprotective effect of sucrose during DEN-induced hepatocarcinogenesis, underlining an intriguing role of high sucrose consumption during HCC development and providing new insights as well as possible pathways of cellular protection under sucrose intake on hepatocarcinogenesis.

Chronic treatment with the antipsychotic lurasidone modulates the neuroinflammatory changes associated with the vulnerability to chronic mild stress exposure in female rats

Stress exposure is a key risk factor for the developmentof depressive-like conditions. However, despite the higher incidence of Major Depressive Disorder in the female population, classical stress-based experimental paradigms have primarily focused on males. In the present study, we used the well-established chronic mild stress (CMS) paradigm to investigate the development of anhedonia, a cardinal symptom of affective disorders, in the female animals and we also studied the potential effect of the antipsychotic drug lurasidone in normalizing the alterations brought about by stress exposure. We found that three weeks of CMS exposure produced a significant reduction of sucrose intake in 50% of the animals (vulnerable, CMS-V), whereas the others were resilient (CMS-R). The development of an anhedonic phenotype in CMS-V was associated with a significant elevation of different immune markers, such as Complement C3 and C4, and inflammatory cytokines, including INFß and Il1ß in dorsal and ventral hippocampus. Interestingly, sub-chronic treatment with the antipsychotic drug lurasidone was able to revert the anhedonic phenotype while normalizing most of the molecular alterations found in rats vulnerable to CMS exposure. This study extends the ability of lurasidone to normalize the anhedonic phenotype in CMS rats also to females. Moreover, we provide novel evidence on lurasidone’s potential effectiveness in treating mental disorders characterized by immune-inflammatory dysfunction.

Unveiling the impact of dietary components on tropomyosin-induced anaphylaxis: Analysis from the perspective of intestinal barrier

There exists a strong correlation between diets and the increased incidence of food allergy. However, the precise mechanism underlying the impact of dietary fat, sucrose, or inulin on tropomyosin (TM)-induced anaphylaxis remains unclear. Therefore, the murine model of TM-induced food allergy fed with a high-fat, high-sucrose, high-dietary-fiber, or control diet was used to explore the mechanism. The high-sucrose diet was found to result in glucose and lipid metabolism disorders, as well as heightened allergic reactions characterized by decreased specific IgG2a levels and increased levels of specific IgE, specific IgG1, IL-4, peritoneal albumin, histamine, and mast cell degranulation. The aggravating impact of a high-fat diet on allergic reactions was weaker than that of a high-sucrose diet. It was attributed to the destruction of the intestinal mucus layer, the decreased expression of zona occludens 1 and occludin, and the increased release of IL-25 and IL-33. Meanwhile, a high sucrose intake led to dysbiosis of intestinal microbiota, and increased the abundance of Roseburia and norank_f_Oscillospiraceae, contributing to a further impairment of intestinal barrier function. Additionally, inulin intake significantly reduced the level of specific IgG1 and peritoneal albumin due to its protective effect on the intestinal barrier. To sum up, a better understanding of the relationship between diet and immune responses will be crucial for developing effective strategies for managing TM-induced food allergy.

7561 Maternal Sucrose Consumption During Gestation Alone Does Not Affect Glucocorticoids and Aldosterone in the Fetal Brain and Blood of Rats

Abstract Disclosure: M.M. Jung: None. D.R. Seib: None. M. Idrissi: None. H.W. Chen: None. K.K. Soma: None. Sucrose (table sugar) is a common added sugar in foods and beverages. Sucrose intake is high worldwide, yet little is known about how sucrose affects the brain and hormones. We designed an isocaloric, macro/micro-nutrient matched control diet (1% kcal sucrose) and high-sucrose diet (26% kcal sucrose) paradigm where the two diets only differ in kcal from sucrose. In this paradigm, maternal high-sucrose diet intake alters glucocorticoids (GCs) which are steroid hormones that regulate numerous physiological processes including the stress response. 16 wk of maternal sucrose intake (10 wk before mating, 3 wk during gestation, and 3 wk during lactation) increases blood and brain corticosterone levels in adult female offspring. Moreover, 13 wk of maternal sucrose intake (10 wk before mating and 3 wk during gestation) increases 11-deoxycorticosterone (DOC, corticosterone precursor) and 11-dehydrocorticosterone (DHC, corticosterone metabolite) in maternal serum, and increases aldosterone in fetal blood and brain at embryonic day 19.5 (E19.5). These results suggest that long-term maternal sucrose intake is a stressor that alters GC and aldosterone signalling. It is unclear whether a maternal high-sucrose diet only during gestation alters fetal steroid levels, or whether long-term sucrose consumption before mating is necessary. Here, we investigate the effects of maternal sucrose intake during gestation only on GCs and aldosterone in the fetal blood and brain. We hypothesize that maternal sucrose intake only during gestation will alter GC and aldosterone signaling in the fetus. We predict that maternal sucrose consumption during gestation alone will increase GC and aldosterone levels in the fetal blood and brain. Female Long-Evans rats were fed either a high-sucrose diet or a control diet starting E0.5 (day of mating confirmation) (n=15/diet). On E19.5, we collected fetal brain and blood and microdissected the regions of the fetal brain that are sensitive to GCs and aldosterone: nucleus accumbens, amygdala, hypothalamus, ventral hippocampus, and ventral tegmental area. We measured a panel of 15 steroids including GCs and aldosterone in the fetal brain (0.8-1.6 mg/region) and blood (5 µL) using liquid chromatography-tandem mass spectrometry, the gold standard for steroid quantification. Maternal high-sucrose diet intake during gestation alone did not alter maternal food intake, maternal body mass, or litter size, but increased the percentage of male offspring per litter. Maternal sucrose intake did not alter DOC, corticosterone, or DHC levels in the fetal blood and brain regions. Aldosterone was not detected in the fetal blood and brain. These results suggest that maternal sucrose intake during gestation alone does not alter GC and aldosterone levels in the developing fetus and that a longer duration of maternal sucrose intake is needed to alter offspring endocrine physiology. Presentation: 6/1/2024

High fat intake aggravates hyperlipidemia and suppresses fatty liver symptoms induced by a high-sucrose diet in rats.

Overconsumption of sucrose or fat is widely acknowledged as a prominent feature of unhealthy dietary patterns. Both factors commonly co-occur and are recognized as hallmarks of the Western diet, which is an important contributor to non-communicative diseases. In this study, we investigated the hazards of high sucrose or fat intake, either alone or in combination. Wistar rats were divided into four groups and fed a control starch diet, high-sucrose diet, high-fat diet, or high-sucrose/fat diet for 30 days. High fat intake increased body weight and visceral and subcutaneous adipose tissue weights. Both high-sucrose and -fat diets were associated with increased plasma triglyceride and glucose levels, and high sucrose also elevated plasma cholesterol levels. The combination of high sucrose and fat synergistically elevated plasma triglyceride levels. The high-sucrose diet increased liver weight and hepatic total lipid and triglyceride levels, whereas this increase was suppressed by the high-fat diet. The high sucrose increased the mRNA levels of hepatic genes involved in fatty acid synthesis and transport (ACLY, ACACA, FAS, ELOVL6, SCD1, SREBP1, and CD36), whereas the high fat suppressed the high sucrose-induced expression of these genes. We observed that high sucrose and fat contents differently exerted their effects on hyperlipidemia and fatty liver. Furthermore, high fat aggravated hyperlipidemia and suppressed fatty liver induced by high sucrose.

Validation of drug-nondrug choice procedure to model maladaptive behavioural allocation to opioid use in rats.

Increased allocation of behaviour to substance abuse at the expense of personal and social rewards is a hallmark of addiction that is reflected in several of DSM-5 criteria for diagnosis of substance use disorder. Previous studies focused on refining the self-administration (SA) model to better emulate an addictive state in laboratory animals. Here, we employed concurrent SA of sucrose pellets and morphine as two competing natural and drug rewards, respectively, to validate the feasibility of capturing pathological behavioural allocation in rats. A custom-made three-lever operant chamber was used. With one active and one inactive lever presented, rats were trained to self-administer morphine (0.5mg/kg/infusion; 2h/day) under a fixed-ratio 1 (FR-1) schedule until a stable response was achieved. Next, they were trained to self-administer morphine in the presence of a third lever dispensing sucrose pellets (20 mg) under FR-1. Concurrent morphine-sucrose SA sessions (2h/day) were continued until stable morphine taking behaviour was re-established. In another experiment, rats first established stable sucrose pellet SA (2h/day, FR-1) and then were trained to take morphine (0.5mg/kg/infusion; 2h/day). Subsequently, all rats underwent extinction training, in which morphine was replaced with saline while sucrose pellets were still available upon lever pressing, followed by cue-induced reinstatement of morphine seeking behaviour. Results showed that rats retained morphine SA when sucrose pellets were also available, but they showed binge-like sucrose intake when morphine was removed during the extinction sessions. However, morphine SA did not develop in rats that had previously established sucrose pellet SA. In conclusion, morphine SA developed even in the presence of a potent competing nondrug reward in rats. Adding an effort-based contingent delivery of a natural reward to the standard SA model, this protocol may provide an improved model of drug addiction in laboratory animals.

Sucrose binge-eating and increased anxiety-like behavior in Sprague–Dawley rats exposed to repeated LPS administration followed by chronic mild unpredictable stress

Exposure to persistent mild stress is a frequently encountered chronic challenge in a rapidly evolving society. Depending on various factors including sex, the response to stressors varies and is closely linked to the phenomenon of resilience. Depression and anxiety can be considered maladaptive responses to such stress. In this rat study, we investigated the sex-dependent effects of low-grade systemic inflammation during 1 week in combination with chronic unpredictable mild stress during the following 4 weeks on anxiety-like behavior and episodic feeding behavior. Increased anxiety-like behavior and increased sucrose intake were identified in stressed compared to control animals regardless of sex. Interestingly, two nearly equally distributed subpopulations were found in the stressed groups within each sex at the end of the 5-week protocol of combined stress exposure: the resistant and the susceptible, which were characterized by unchanged and increased sucrose intake, respectively. This difference in susceptibility to protracted combined mild stress and ensuing response to a sucrose eating binge demonstrates the complexity of the underlying regulatory mechanisms associated with emotional hyperreactivity. This model carries the potential for further investigation of the molecular basis of resilience and susceptibility to combined stressors and for testing treatments with potential preventive or therapeutic effects.

Melatonin alleviates LPS-induced depression-like behavior in mice by inhibiting ferroptosis by regulating RNA methylation-mediated SIRT6/Nrf2/HO-1 pathway.

The objective of this study is to investigate the impact of ferroptosis on depression and elucidate the molecular mechanism underlying melatonin's inhibitory effect on ferroptosis in the treatment of depression. In this study, a depression-like behavior model was induced in mice using LPS, and the effect of melatonin on depression-like behavior was evaluated through behavioral experiments (such as forced swimming test (FST) and sucrose preference test (SPT)). Additionally, molecular biological techniques (including real-time fluorescence quantitative PCR, Western blotting, immunoprecipitation) were employed to detect the expression levels and interactions of METTL3, SIRT6 and ferroptosis-related genes in mouse brain tissue. Furthermore, both in vitro and in vivo experiments were conducted to verify the regulatory effect of melatonin on Nrf2/HO-1 pathway and explore its potential molecular mechanism for regulating ferroptosis. Melatonin was found to significantly ameliorate depression-like behavior in mice, as evidenced by reduced immobility time in the forced swimming test and increased sucrose intake in the sucrose preference test. Subsequent investigations revealed that melatonin modulated SIRT6 stability through METTL3-mediated ubiquitination of SIRT6, leading to its degradation. As a deacetylase, SIRT6 plays a pivotal role in cellular metabolism regulation and antioxidative stress response. This study elucidated potential signaling pathways involving Nrf2/HO-1 through which SIRT6 may exert its effects. The findings suggest that melatonin can improve depressive behavior by suppressing ferroptosis and protecting neurons through its antioxidant properties. Additionally, targeting the Nrf2/HO-1 pathway via METTL3 and NEDD4 regulation may be a potential therapeutic approach for depression.

Biosynthesis of nonnutritive monosaccharide d-allulose by metabolically engineered Escherichia coli from nutritive disaccharide sucrose.

Sucrose is a commonly utilized nutritive sweetener in food and beverages due to its abundance in nature and low production costs. However, excessive intake of sucrose increases the risk of metabolic disorders, including diabetes and obesity. Therefore, there is a growing demand for the development of nonnutritive sweeteners with almost no calories. d-Allulose is an ultra-low-calorie, rare six-carbon monosaccharide with high sweetness, making it an ideal alternative to sucrose. In this study, we developed a cell factory for d-allulose production from sucrose using Escherichia coli JM109 (DE3) as a chassis host. The genes cscA, cscB, cscK, alsE, and a6PP were co-expressed for the construction of the synthesis pathway. Then, the introduction of ptsG-F and knockout of ptsG, fruA, ptsI, and ptsH to reprogram sugar transport pathways resulted in an improvement in substrate utilization. Next, the carbon fluxes of the Embden-Meyerhof-Parnas and the pentose phosphate pathways were regulated by the inactivation of pfkA and zwf, achieving an increase in d-allulose titer and yield of 154.2% and 161.1%, respectively. Finally, scaled-up fermentation was performed in a 5 L fermenter. The titer of d-allulose reached 11.15 g/L, with a yield of 0.208 g/g on sucrose.

Clinical Evaluation of the Effect of Nanohydroxyapatite Lozenge on the pH of Dental Plaque.

This study investigated the influence of nanohydroxyapatite-containing (nanoHAP) lozenge on plaque pH following sucrose intake. Sixteen adult subjects were enrolled in this double-blind crossover study composed of four interventions: (1) 10% w/v sucrose solution, (2) 10% w/v sorbitol solution, (3) nanoHAP lozenge, and (4) 10% w/v sucrose solution challenge followed by nanoHAP lozenge. Following the determination of each subject's resting plaque pH, the pH was measured at different time intervals from 3 to 30 minutes from the start of intervention, with 7 days interval between the applications of different interventions. The data were analyzed using the analysis of variance and Tukey's test (α < 0.05). While sorbitol produces no change in plaque pH, nanoHAP-lozenge increased the plaque pH from a baseline of 7.0 ± 0.3 (mean ± sd) to 7.8 ± 0.2 (mean ± sd) within 30 minutes. Sucrose lowered the plaque pH from a baseline of 7.0 ± 0.4 (mean ± sd) to the lowest minimum of 5.1 ± 0.1 (mean ± sd) at the 7th minute, rising above the critical pH of enamel dissolution (5.5) at 12th minute and the baseline pH in more than 30 minutes. With lozenge intervention following sucrose challenge, plaque pH rose to 5.5 in 8 min, and to the baseline pH in 24 min. The cH area (Hydrogen ion concentration area) produced by sucrose (1.82 sq. units) was significantly (p < 0.05) greater than that produced when sucrose was challenged with lozenge (0.48 sq. units). Nanohydroxyapatite-containing lozenge increased plaque pH, reduced plaque pH drop in the presence of sucrose, and facilitated the rapid recovery of plaque pH after sucrose intake.

P171 WATER DEPRIVATION REDUCES WATER INTAKE AND INCREASES SUCROSE INTAKE IN SPONTANEOUSLY HYPERTENSIVE RATS: POSSIBLE MECHANISMS

Background and Objective: Water deprivation (WD), a common situation in wild and human lives, can induce an increase in sucrose palatability in SHR. However, it is not known if SHR also has an increase in sucrose intake after WD and if this intake is related to energy intake, as WD reduces food intake, or to the change in sucrose palatability. Methods: Adult (∼12 weeks) male Holtzman (normotensive, NT) or SHR rats (n = 20/strain) were used. In protocol 1, all rats were first subjected to 24-h WD. Food consumption was measured during WD and was used for the non-water deprived (ND)/food restricted (FD) group to equal energy consumption. Three days after the WD, rats were randomly assigned to the 24-hour WD or the ND/FR group. In protocol 2, animals were implanted with an intraoral cannula and were randomly assigned as above. Results: In the WD condition, water intake was greater in NT (15.9 ± 1.1, vs. SHR: 8.6 ± 0.2 mL/120 min, p &lt; 0.05), whereas sucrose intake was greater in SHR (8.8 ± 0.7, vs. NT: 2.1 ± 1 mL/120 min, p&lt; 0.05). In the ND/FR condition, water intake was very low in both strains, however, SHR had a higher sucrose intake compared to NT (11.5 ± 2.0, vs. NT: 3.3 ± 1.8 mL/120 min; p &lt; 0.05). In NT rats, in the WD condition, there was a decrease in sucrose palatability compared to the ND/FR condition, whereas in SHR palatability was similar in the WD or ND/FR condition. SHR have a greater mean arterial pressure than NT (167 ± 3 vs, NT: 105 ± 2 mmHg). Conclusions: Our results suggest that SHR favours energy intake during WD, since during ND/FR they drank equivalent amount of sucrose. This suggestion is supported by the absence of a greater palatability to sucrose in SHR when food is restricted. Support: CAPES PrINT, FAPESP, CNPq

Chronic sleep restriction during juvenility alters hedonic and anxiety-like behaviours in a sex-dependent fashion in adolescent Wistar rats.

Chronic reduction of sleep time in children and adolescents has been related to increased incidence of anxiety and depression. In rats, protocols of protracted sleep deprivation or chronic sleep restriction (CSR) are considered a stressor. In previous studies we showed that post-weaning CSR in male rats induces anxiety-like behaviour and changes in neurotransmission in emotion-related brain areas. In the present study we examined whether the effects of this adversity are sex-dependent. Twenty-two litters, containing four males and four females were distributed into control (CTL) and CSR groups. CSR began on postnatal day (PND) 21 and lasted for 21 days; each day the animals were placed onto small platforms immersed in water for 18 h and were allowed to sleep freely in their home-cages for the remaining 6 h. Throughout the CSR, all animals underwent the sucrose splash test once/week to assess their self-care and hedonic behaviours. Body weight was measured on PNDs 21 and 42. At the end of CSR period, the adolescents were allowed to sleep freely for 2 days, after which, behavioural tests began. Within each litter, one male and one female (pair) were not tested and provided blood and brain for determination of basal corticosterone (CORT) levels and hippocampal BDNF. One pair was tested in the sucrose preference test (SPT), one pair on the elevated plus maze (EPM) and one pair in the forced swim test (FST). CORT was measured after all conditions. CSR impaired self-care behaviour and body weight gain in males and females and increased relative adrenal weight only in males. There were no changes in sucrose intake in the SPT; CSR females displayed less immobility in the FST and CSR males displayed more anxiety-like behaviour in the EPM. CORT levels were similar between CTL and CSR males, whilst lower in CSR females than CTL ones in all experimental conditions. No changes in BDNF levels were detected in the dorsal hippocampus of CSR rats. The results indicate that CSR impaired self-care behaviour in both sexes, but only males displayed anxiety-like behaviour, whilst sleep recovery in females appeared to normalise their behaviour.

Sex-specific differences in NAFLD development: effect of a high-sucrose diet on biochemical, histological, and genetic markers in C57bl/6N mice

ABSTRACT Sucrose intake is a potential risk factor for non-alcoholic fatty liver disease (NAFLD). Individual characteristics such as sex, play arole in the biological variation of the disease, potentially related to genetic regulation. This research evaluated sex differences in biochemical, histopathological, and gene expression responses associated with NAFLD in C57bl/6N mice on a high sucrose diet. Female and male mice were assigned to control or high sucrose diets (50% sucrose solution) for 20 weeks. After sacrifice, blood and hepatic tissue were collected for analysis. Female mice revealed moderate-to-high NAFLD, whereas male mice showed mild-to-moderate NAFLD. Sex-specific variations were observed in Cd36 gene expression, an upregulation in females compared with the male group, and Adipor1 gene expression showed significant downregulation in the female group in response to high sucrose diet compared with the control group. These findings highlight the importance of considering gender disparities in the treatment and management of NAFLD.

Palatable solution overconsumption in the Cntnap2-/- murine model of autism: a link with oxytocin.

Dysregulated appetite is common in autism spectrum disorder (ASD) and it includes excessive interest in tasty foods. Overconsumption of palatable fluids has been found in the valproic acid-induced ASD rat. Though ASD has a strong genetic component, the link between ASD-related genes and appetite for palatable foods remains elusive. We focused on the CNTNAP2 gene whose deletion in mice recapitulates human ASD symptoms. We investigated whether Cntnap2-/- male mice consume greater amounts of palatable 10% sucrose, 0.1% saccharin, and 4.1% intralipid solutions offered in episodic meals either in a no-choice paradigm or a two-bottle choice test. We examined how sucrose intake affects c-Fos immunoreactivity in feeding-related brain areas. Finally, we determined doses at which intraperitoneal oxytocin decreases sucrose intake in mutants. In the single-bottle tests, Cntnap2-/- mice drank more sucrose, saccharin, and intralipid compared to WTs. Given a choice between two tastants, Cntnap2-/- mice had a higher preference for sucrose than intralipid. While the standard 1 mg/kg oxytocin dose reduced sucrose intake in WTs, a low oxytocin dose (0.1 mg/kg) decreased sucrose intake in Cntnap2-/- mice. Sucrose intake induced a more robust c-Fos response in wild-type (WT) than Cntnap2-/- mice in the reward and hypothalamic sites and it increased the percentage of Fos-immunoreactivity oxytocin neurons in WTs, but not in mutants. We conclude that Cntnap2-/- mice overconsume palatable solutions, especially sucrose, beyond levels seen in WTs. This excessive consumption is associated with blunted c-Fos immunoreactivity in feeding-related brain sites, and it can be reversed by low-dose oxytocin.

Don't ignore the middle: Distinct mnemonic functions of intermediate hippocampus.

The dorsal region of the hippocampus (dHC) mediates many of the mnemonic functions traditionally associated with the hippocampus proper, such as spatial and episodic memory, whereas ventral hippocampus (vHC) has been extensively implicated in emotional memory and motivational processes. By contrast, the functions of the intermediate hippocampus (iHC) are far less understood. In this study, we aimed to investigate the mnemonic functions of iHC by reversibly inactivating iHC prior to testing memory in behavioral tasks dependent on the integrity of dHC, iHC, or vHC, namely, rapid place water maze, inhibitory avoidance, spontaneous alternation, and temporal ordering of odors. Given our previous findings showing that dHC and vHC are involved in mnemonic control of ingestive behavior, we also assessed the effects of iHC inactivation on sucrose intake. The results showed that pharmacological inhibition of iHC impairs rapid place water maze memory, which has been previously shown to be dependent on iHC but not dHC or vHC. iHC inactivation does not impact memory dependent on dHC (spontaneous alternation), vHC (temporal odor memory), or either dHC or vHC (inhibitory avoidance), and only modestly affects sucrose intake. These findings provide support for the involvement of iHC in mnemonic functions that are distinct from dHC and vHC and highlight the need to further advance our understanding of the functions of this hippocampal region that has been relatively understudied.

Impact of excessive sucrose intake on mouse behavior across different developmental stages.

This study aimed to elucidate the effects of sucrose (SUC) consumption on neurodevelopmental processes through behavioral changes in rodents and determine whether these effects could be because of sweet taste, energy supply, or both. Mice were divided into five groups based on the time of SUC or sucralose (SUR, a noncaloric sweetener) administration: for 6 days from gestation day (GTD) 7, to birth from GTD13 and for 15 days from postnatal day (PND) 21, PND38, and PND56. SUC and SUR administration did not impact body weight. However, food intake in the PND56 group and water intake in the GTD13 and PND56 groups were increased by SUC and SUR administration. Amphetamine (0.5, 1, 2, and 3 mg/kg), a dopamine reuptake inhibitor, administration to assess alterations in the dopaminergic system induced increases in distance traveled after SUC administration in the GTD13 and PND21 groups compared with that in the control (vehicle administration) group. In contrast, the SUR group showed a decrease in the distance traveled in the PND56 group. Although there were no differences in locomotor activity and foraging behavior, SUC preference increased in the SUC group regarding the GTD13 and PND38 groups. The correlations between SUC preference and foraging behavior and between SUC preference and amphetamine response varied in both groups according to the developmental stage. Excessive SUC consumption might affect neural function at different developmental stages, as it could affect brain function through complex mechanisms involving sweet taste and energy supply and influence the dopaminergic system.

Are dietary factors associated with cardiometabolic risk factors in patients with non-alcoholic fatty liver disease?

Non-alcoholic fatty liver disease (NAFLD) is intricately linked with dietary patterns and metabolic homeostasis. Therefore, the present study focused to investigate the relation between dietary patterns and cardiometabolic risk factors related to fatty liver in NAFLD patients. This cross-sectional study included 117 individuals whose body mass index (BMI) threshold of 25 or above diagnosed with NAFLD by magnetic resonance imaging. The hospital database was used to review the patients' medical records such as lipid parameters, and fasting blood sugar. Anthropometric measurements and body composition were measured by researchers. Likewise, data from 24-h dietary recalls of individuals were collected to analyze their energy and nutrient intakes besides calculating dietary insulin index (DII), dietary insulin load (DIL), dietary glycemic index (DGI), and dietary glycemic load (DGL). Participants consuming diets with distinct levels of DII, DIL, DGI, and DGL exhibited variations in dietary energy and nutrient intake. Specifically, differences were noted in carbohydrate intake across quartiles of DII, DIL, DGI, and DGL, while fructose consumption showed variability in DGL quartiles (p ≤ 0.05). Moreover, sucrose intake demonstrated distinctions in both DII and DGL quartiles (p ≤ 0.05). No statistical difference was found in biochemical parameters and the fatty liver index among different levels of DII, DIL, DGI, and DGL (p > 0.05). After adjusting for potential confounders, participants with a higher DGI had four times greater odds of developing metabolic syndrome compared to those in the bottom quartile (OR, 4.32; 95% CI [1.42-13.11]). This study provides initial evidence of the intricate association between dietary factors and NAFLD, emphasizing the necessity for further research including prospective designs with larger sample sizes, to garner additional insights.