Consumption Of Sucrose Solution Research Articles

IPM Strategy to Control EFB in Apis mellifera: Oxytetracycline Treatment Combined with Partial Shook Swarm and Queen Caging.

We tested an integrated pest management (IPM) strategy to control European foulbrood (EFB) in honey bees. Colonies affected by EFB were assigned to two homogenous groups: an oxytetracycline-treated group (1.5 g OTC/hive) that underwent partial shook swarm (PSS) in combination with queen caging (QC) and an untreated group where only two beekeeping techniques, PSS and QC, were applied. The consumption of sucrose solution, the strength of the colonies, side effects of the mentioned techniques, clinical as well as subclinical relapses of EFB, and the amount of OTC residues in the honey were assessed over a 7-month-long monitoring period. Regarding the consumption of the sucrose solution, there was no significant difference between the OTC-treated and untreated groups. The strength of the untreated colonies was consistently but not significantly higher than those treated with OTC. PSS combined with QC resulted in various side effects in both groups: queen loss (52%), absconding (8%), and drone-laying queen (4%). Untreated colonies (16.7%) showed clinical EFB relapses 4 months after the application of PSS along with QC, while 15.4% of the OTC-treated colonies were confirmed EFB-positive by PCR. OTC residues were detected in the honey yielded in the cases of both groups. Two months after the PSS, the amount of OTC residues in the untreated group was 0.6 ± 0.2 µg/kg, while that in the OTC-treated group amounted to 5.8 ± 11.6 µg/kg; both results are below the maximum residue limit (MRL) of 100 ppb considered in the EU for cascade use.

The Neonicotinoid Imidacloprid Impairs Learning, Locomotor Activity Levels, and Sucrose Solution Consumption in Bumblebees (Bombus terrestris).

Bumblebees carry out the complex task of foraging to provide for their colonies. They also conduct pollination, an ecosystem service of high importance to both wild plants and entomophilous crops. Insecticides can alter different aspects of bumblebee foraging behavior, including the motivation to leave the hive, finding the right flowers, handling flowers, and the ability to return to the colony. In the present study, we assessed how the neonicotinoid imidacloprid affects bumblebees' foraging behavior after exposure to four different treatment levels, including field-realistic concentrations (0 [control], 1, 10, and 100 μg/L), through sucrose solution over 9 days. We observed the behavior of several free-flying bumblebees simultaneously foraging on artificial flowers in a flight arena to register the bees' complex behavior postexposure. To conduct a detailed assessment of how insecticides affect bumblebee locomotor behavior, we used video cameras and analyzed the recordings using computer vision. We found that imidacloprid impaired learning and locomotor activity level when the bumblebees foraged on artificial flowers. We also found that imidacloprid exposure reduced sucrose solution intake and storage. By using automated analyses of video recordings of bumblebee behavior, we identified sublethal effects of imidacloprid exposure at field-realistic doses. Specifically, we observed negative impacts on consumption of sucrose solution as well as on learning and locomotor activity level. Our results highlight the need for more multimodal approaches when assessing the sublethal effects of insecticides and plant protection products in general. Environ Toxicol Chem 2023;42:1337-1345. © 2023 SETAC.

Sugar-sweetened beverages exacerbate high-fat diet-induced inflammatory bowel disease by altering the gut microbiome

High-fat diets (HFDs) and frequent consumption of sugar-sweetened beverages (SSBs) are potential contributors to increasing inflammatory bowel disease (IBD) incidences. While HFDs have been implicated in mild intestinal inflammation, the role of sucrose in SSBs remains unclear. Therefore, we studied the role of SSBs in IBD pathogenesis in a mouse model and humans. C57BL6/J mice were given ad libitum access to a sucrose solution or plain water for 10 weeks, with or without an HFD. Interestingly, sucrose solution consumption alone did not induce gut inflammation in mice; however, when combined with an HFD, it dramatically increased the inflammation score, submucosal edema, and CD45+ cell infiltration. 16S ribosomal RNA gene-sequencing revealed that sucrose solution and HFD co-consumption significantly increased the relative abundance of IBD-related pathogenic bacteria when compared with HFD consumption. RNA sequencing and flow cytometry showed that co-consumption promoted pro-inflammatory cytokine and chemokine synthesis, dendritic-cell expansion, and IFN-γ+TNF-α+CD4+ and CD8+ T-cell activation. Fecal microbiota transplantation from HFD- and sucrose water-fed mice into gut-sterilized mice increased the susceptibility to dextran sulfate sodium-induced colitis in the recipient mice. Consistent herewith, high consumption of SSBs and animal fat-rich diets markedly increased systemic inflammation-associated IBD marker expression in humans. In conclusion, SSBs exacerbate HFD-induced colitis by triggering a shift of the gut microbiome into a pathobiome. Our findings provide new insights for the development of strategies aimed at preventing IBD.

Investigating the effects of glyphosate on the bumblebee proteome and microbiota

Glyphosate is one of the most widely used herbicides globally. It acts by inhibiting an enzyme in an aromatic amino acid synthesis pathway specific to plants and microbes, leading to the view that it poses no risk to other organisms. However, there is growing concern that glyphosate is associated with health effects in humans and an ever-increasing body of evidence that suggests potential deleterious effects on other animals including pollinating insects such as bees. Although pesticides have long been considered a factor in the decline of wild bee populations, most research on bees has focussed on demonstrating and understanding the effects of insecticides. To assess whether glyphosate poses a risk to bees, we characterised changes in survival, behaviour, sucrose solution consumption, the digestive tract proteome, and the microbiota in the bumblebee Bombus terrestris after chronic exposure to field relevant doses of technical grade glyphosate or the glyphosate-based formulation, RoundUp Optima+®. Regardless of source, there were changes in response to glyphosate exposure in important cellular and physiological processes in the digestive tract of B. terrestris, with proteins associated with oxidative stress regulation, metabolism, cellular adhesion, the extracellular matrix, and various signalling pathways altered. Interestingly, proteins associated with endocytosis, oxidative phosphorylation, the TCA cycle, and carbohydrate, lipid, and amino acid metabolism were differentially altered depending on whether the exposure source was glyphosate alone or RoundUp Optima+®. In addition, there were alterations to the digestive tract microbiota of bees depending on the glyphosate source No impacts on survival, behaviour, or food consumption were observed. Our research provides insights into the potential mode of action and consequences of glyphosate exposure at the molecular, cellular and organismal level in bumblebees and highlights issues with the current honeybee-centric risk assessment of pesticides and their formulations, where the impact of co-formulants on non-target organisms are generally overlooked.

Fibroblast growth factor 21 and dietary macronutrient intake in female mice

Fibroblast growth factor- 21 (FGF21) is a metabolic stress hormone that is released from the liver in response to various nutritional challenges. Because of its notable effects to improve metabolic health, including body fat loss, glucose control, and hepatosteatosis, several pharmaceutical analogs of FGF21 are in development for the treatment of metabolic disease. In addition, a small but developing literature clearly demonstrates that FGF21 also controls feeding behavior. Pharmacological administration of FGF21 reduces the consumption of simple sugars and other sweet tastants, and it increases the consumption of dietary proteins in males, suggesting another potential mechanism by which FGF21-treatment could improve metabolic health— by promoting healthy eating. Despite that sex is a key biological variable influencing feeding behavior and macronutrient selection, the current literature to date primarily on males. In this study, we investigated the effect of FGF21 on sucrose intake and macronutrient selection in female mice. Similar to our previous findings in male mice, we report that FGF21 administration decreases the consumption of sucrose solution by females, and that this is offset by increased chow intake. Also in agreement with our previous findings in males, we report that FGF21 increases the consumption of dietary protein by female mice, and this is offset by either reduced carbohydrate or by reduced fat intake. Lastly, we find that the effect of FGF21 to direct macronutrient intake in females depends on its actions in neurons. Overall, our data support a role for FGF21 to direct macronutrient intake in a similar manner in female and male mice.

Ginsenoside Rb1 Produces Antidepressant-Like Effects in a Chronic Social Defeat Stress Model of Depression Through the BDNF–Trkb Signaling Pathway

Ginsenoside Rb1 (Rb1), an important bioactive ingredient of Panax ginseng, has potent neuroprotective effects. The objective of the study is to elucidate the impact of Rb1 treatment on chronic social defeat stress (CSDS)–induced depressive-like behaviors and its related mechanism. According to the obtained results, the daily oral administration of Rb1 (35 and 70 mg/kg) and imipramine (15 mg/kg) for 28 days significantly reversed the social avoidance behavior, anhedonia, and behavioral despair via CSDS exposure, as demonstrated by the considerable elevation in the time in the zone in the social interaction test, consumption of sucrose solution in the sucrose preference test, and decrease in immobility time in the forced swim test. Moreover, Rb1 obviously restored the CSDS-induced decrease in the BDNF signaling pathway and hippocampal neurogenesis. Rb1 significantly increased the hippocampal levels of ERK, AKT, and CREB phosphorylation and increased the number of DCX+ cells in DG. Importantly, the antidepressant effects of Rb1 were completely blocked in mice by using K252a (the nonselective tyrosine kinase B inhibitor). In conclusion, our results indicated that Rb1 exerts promising antidepressant-like effects in mice with CSDS-induced depression, and its effects were facilitated by enhancing the BDNF signaling cascade and upregulation of hippocampal neurogenesis.

Inhibition of serotonergic signaling induces higher consumption of both sucrose solution and toxic baits in carpenter ants

Biogenic amines play an important role in the regulation of appetitive responses in insects. Among them, serotonin (5-HT) regulates feeding-related processes in numerous insect species. In carpenter ants, 5-HT administration has been shown to depress feeding behavior, thus opening the possibility of using 5-HT modulation in control strategies against those species considered as pest. Here we studied if administration of a 5-HT antagonist, ketanserin, promotes feeding of a sucrose solution and a toxic bait in carpenter ants Camponotus mus. We found that 3 h after a single oral administration of ketanserin, the mass of sucrose solution consumed by carpenter ants increased significantly. A similar effect was found after a chronic administration that lasted 5 days. Yet, ketanserin did neither affect the intake rates nor the activity of the pharyngeal pump that mediates feeding dynamics. In addition, ketanserin promoted the consumption of a toxic bait based on boric acid. Our results thus show that feeding motivation and consumption of both sucrose solution and a toxic bait can be enhanced via prior administration of ketanserin. We discuss the possible mechanisms underlying these effects and conclude that understanding basic physiological and neural principles that underlie feeding motivation allows establishing more efficient control strategies for pest insects.

Lateral hypothalamus-projecting noradrenergic locus coeruleus pathway modulates binge-like ethanol drinking in male and female TH-ires-cre mice

A growing body of literature implicates noradrenergic (NE) signaling in the modulation of ethanol consumption. However, relatively few studies have detailed specific brain pathways that mediate NE-associated binge-like ethanol consumption. To begin to fill this gap in the literature, male and female C57BL6/J and TH-ires-cre mice underwent pharmacological and chemogenetic testing, respectively, in combination with “drinking in the dark” procedures to model binge-like consumption of ethanol or sucrose solutions. First, we showed that intraperitoneal administration of the NE reuptake inhibitor, reboxetine, blunted binge-like ethanol intake in C57BL6/J mice. Chemogenetic activation of locus coeruleus (LC) tyrosine hydroxylase (TH)-expressing neurons blunted binge-like ethanol intake regardless of sex. Chemogenetic activation of LC projections to the lateral hypothalamus (LH), a region implicated in ethanol consumption, blunted binge-like ethanol drinking without altering sucrose intake in ethanol-experienced or ethanol-naïve mice. In C57BL/6 J mice, LH-targeted microinfusion of an α1-adrenergic receptor (AR) agonist blunted binge-like ethanol intake across both sexes, while LH infusion of a β-AR agonist blunted binge-like ethanol intake in females exclusively. Finally, in mice with high baseline ethanol intake both an α1- AR agonist and an α-2 AR antagonist blunted binge-like ethanol intake. The present results provide novel evidence that increased NE tone in a circuit arising from the LC and projecting to the LH reduces binge-like ethanol drinking in mice, and may represent a novel approach to treating binge or heavy drinking prior to the development of dependence.This article is part of the special Issue on “Neurocircuitry Modulating Drug and Alcohol Abuse”.

Fecal microbiota transplantation ameliorates gut microbiota imbalance and intestinal barrier damage in rats with stress-induced depressive-like behavior.

The gut-microbiota-brain axis is the most important complex and bidirectional pathway between the gastrointestinal tract and the central nervous system. This study investigated the potential of microbe-induced gut-to-brain signaling to modulate the effect of stress on depressive-like behavior, intestinal barrier, and neuroinflammation. Result showed that fecal microbiota transplantation increased the consumption of sucrose solutions and decreased the immobility time in forced swimming test. This treatment also increased Firmicutes and decreased Bacteroidetes and Desulfobacterota at phylum levels; reduced the loss of villi and epithelial cells; suppressed the inflammatory cell infiltration in the ileum; increased the expression of ZO-1, occludin; protected the mucosal layer function; and suppressed the high levels of inflammasomes (NLRP3, ASC, caspase-1, and IL-1β) in rat brain. In summary, fecal microbiota transplantation improves the depressive-like behavior, alters the gut microbiota imbalance, and alleviates the intestinal tract inflammation, intestinal mucosa disruption, and neuroinflammation in rats induced by chronic unpredictable mild stress.

Effects of Original Compounds GSB-106, GML-3, and GZK-111 in an Experimental Lipopolysaccharide-Induced Anhedonia Model

Antidepressant activities of the original compounds GSB-106 [bis(N-monosuccinyl-L-seryl-L-lysine) hexamethylenediamide], a mimetic of the fourth loop of brain-derived neurotrophic factor (BDNF); GML-3(N-butyl-N-methyl-1-phenylpyrrolo[1,2-a]pyrazine-3-carboxamide), a ligand of 18 kDa translocator protein (TSPO); and GZK-111 (N-phenylacetylglycyl-L-proline ethyl ester), a substitute dipeptide that is biotransformed into the neuropeptide cyclo-L-prolylglycine that affects AMPA receptors; were previously revealed at V. V. Zakusov Institute of Pharmacology in experimental models of the depressive state caused by unescapable stress conditions. The present article studied the antidepressant effects of GSB-106, GML-3, and GZK-111 in an inflammatory model of the depressive state induced by lipopolysaccharide (LPS) in male C57Bl/6 mice with an assessment of anhedonia based on the consumption of sucrose solution. LPS in a single dose of 0.5 mg/kg intraperitoneally (i.p.) caused a marked decrease of 39% (p ≤ 0.01) in the consumption of 1% sucrose solution as compared to the control group. GSB-106 administered perorally at a dose of 0.5 mg/kg 24 h after LPS increased by 20% (p ≤ 0.05) sucrose consumption reduced by LPS in mice. GML-3 administered once perorally at doses of 0.5 and 1.0 mg/kg increased sucrose consumption by 29 and 21% (p ≤ 0.01), respectively. GZK-111 administered once i.p. at a dose of 1.0 mg/kg increased sucrose consumption by 17% (p ≤ 0.05). The obtained data confirmed the antidepressant properties of GSB-106, GML-3, and GZK-111.

Reduced caloric intake allows access-induced consumption differences to emerge with concentrated sucrose solutions

Rats given intermittent access to 4% (w/v) sucrose solution elevate their consumption of solution relative to rats with continuous access, a difference that does not appear at higher concentrations. Here, we examined the hypothesis that a limit on the intake of sucrose calories prevents rats from demonstrating access-induced differences in consumption of a more concentrated sucrose solution. Energy-replete rats were given every day (ED) or every third day (E3D) access to sucrose solutions adulterated with bitter quinine which reduced solution palatability and consumption levels while intake was measured. In experiment 1, previously collected data were compiled to examine the trajectory of consumption of continuously available 4% sucrose solution which was shown to stabilize by day 3 and then informed group assignment. In experiment 2, daily consumption levels were higher for rats with E3D access to 4% sucrose solution than rats with ED access to the same solution, whereas rats consumed similar amounts of 8% sucrose solution across access schedules. In the first hour of solution availability rats with E3D access showed elevated sucrose solution consumption, relative to rats with ED access, for both 4% and 8% sucrose solution. Upon the addition of quinine (0.005%) sucrose solution consumption decreased and the E3D access group consumed more daily sucrose solution than the ED access group for both 4% and 8% sucrose solution. In experiment 3, four groups of rats were given ED or E3D access to 8% sucrose solution adulterated with 0.0025%, 0.005%, 0.01%, or 0.02% quinine. Quinine adulteration reduced 8% sucrose solution consumption and allowed rats with E3D access to elevate their consumption levels relative to rats with ED access; this effect persisted when all groups were switched to 8% sucrose + 0.02% quinine solution. Thus, daily access-induced consumption differences develop but do not emerge because of a caloric limit on sucrose solution intake. This work underscores the interaction of availability and caloric intake as determinants of sugar consumption and highlights an important distinction between animal models of food addiction and binge eating.

Fluoxetine and Ketamine Reverse the Depressive but Not Anxiety Behavior Induced by Lesion of Cholinergic Neurons in the Horizontal Limb of the Diagonal Band of Broca in Male Rat.

The basal forebrain cholinergic system is involved in cognitive processes, but the role of the basal forebrain cholinergic system in depression is unknown. We investigated whether a lesion of cholinergic neurons in the horizontal limb of the diagonal band of Broca (HDB) produces depressive-like behavior and whether fluoxetine or ketamine inhibits such depressive-like behaviors. Here, in rats, we used 192 IgG-saporin to eliminate the cholinergic neurons of the HDB and evaluated depressive-like behaviors using a preference test for sucrose solution and the forced swimming test. Fourteen days after the injection of 192 IgG-saporin into the HDB, the rats exhibited a significantly fewer number of choline acetyltransferase positive cell density in HDB, accompanied with neuronal loss in the entire hippocampus. Meanwhile, these rats significantly reduced preference for sucrose solution, increased immobility time in the forced swimming test, reduced locomotor activity, decreased context dependent memory in fear conditioning and the time spent in the open arms of the plus-maze. A single dose of ketamine (10 mg/kg) increased the sucrose solution consumption, reduced the immobility time in the forced swim test (FST), and increased locomotor activity compared to vehicle-treated rats. Moreover, in rats that were continuously treated with fluoxetine (10 mg/kg/day for 11 days), the sucrose solution consumption increased, the immobility time in the FST decreased, and locomotor activity increased compared to vehicle-treated rats. The present results demonstrate that a lesion of HDB cholinergic neurons results in depressive-like and anxiety-like behaviors and that antidepressants such as fluoxetine or ketamine, can reverse these depressive-like behaviors but not anxiety-like behaviors, and suggest that a lesion of HDB cholinergic neurons and followed hippocampus damage may be involved in the pathogenesis of depression.

Grape seed proanthocyanidins improves depression-like behavior by alleviating oxidative stress and NLRP3 activation in the hippocampus of prenatally-stressed female offspring rats

ABSTRACT Over several decades, there is a growing evidence, which has shown that prenatal stress (PS) contributes to depression in offspring. Grape seed proanthocyanidins (GSPs), which contain dimers, trimers, oligomers of catechin and epicatechin, are known to possess antidepressant effects. The present study aimed to investigate the mechanism of antidepressant effects of GSPs on female juvenile prenatally stressed offspring rats. The results showed that the female juvenile offspring rats exposed to PS exhibited depression-like behavior manifested as longer immobility time and lesser consumption of sucrose solution. Prenatal stress reduced the number of hippocampal neurons and increased the level of the reactive oxygen species (ROS) in the hippocampus of the female juvenile offspring rats. Furthermore, the expression of PYD domains-containing protein 3 (NLRP3) and its downstream cytokines, Caspase-1, and interleukin-1β (IL-1β), were increased in the hippocampus of the female juvenile offspring rats exposed to PS. Administration of GSPs not only improved depression-like behavior and enhanced the number of hippocampal neurons, but also abated excessive ROS generation and inhibited the activation of the NLRP3-Caspase-1 signaling pathway. Taken together, GSPs counteract PS-induced hippocampal neuron loss and depression-like behavior by alleviating oxidative stress and NLRP3 activation. The present study provides a new insight for GSPs as an effective therapeutic agent for adolescent depression.

Effect of Tongdu Tiaoshen acupuncture on PI3K/Akt/mTOR signaling pathway and autophagy-related proteins of hippocampus in rats with post-stroke depression

To observe the improvement of Tongdu Tiaoshen acupuncture on depression-like behavior in rats with post-stroke depression (PSD), and to explore its possible mechanism. A total of 48 SD rats were randomized into a sham-operation group, a model group, a Tongdu Tiaoshen group and a non-meridian-non-acupoint group, 12 rats in each group. In the the model group, the Tongdu Tiaoshen group and the non-meridian-non-acupoint group, PSD model was established by the compound method of cerebral medial arterial occlusion, chronic unpredictable mild stress and isolation. Acupuncture was applied at "Dazhui"(GV 14), "Shuigou"(GV 26), "Baihui"(GV 20) and "Shenting" (GV 24) in the Tongdu Tiaoshen group, and at the bilateral dorsum hollows between 3rd and 4th metatarsal bones of the forelegs in the non-meridian-non-acupoint group, needles were retained for 40 min in the both groups, once a day, 6 times a week for 4 weeks. Before model establishment and after intervention, the ethology indice of Zea Longa neurological behavioral score, open-field test and sucrose preference test were evaluated in the 4 groups. The levels of phosphatidylinositol 3-kinase (PI3K), phosphorylated protein kinase B (p-Akt), phosphorylated mammalian target of rapamycin (p-mTOR), Beclin1 and LC3B-Ⅱ/Ⅰin the CA1 region of hippocampus were detected by western blot. The expressions of Beclin1, LC3B-ⅡmRNA in the CA1 region of hippocampus were detected by real-time PCR. After model established, compared with the sham-operation group, the Zea Longa neurological behavioral scores were increased (P<0.05), the scores of horizontal and vertical motion of the open-field test and the consumption of sucrose solution were decreased in the model group, the Tongdu Tiaoshen group and the non-meridian-non-acupoint group (P<0.05). After intervention, compared with the sham-operation group, the Zea Longa neurological behavioral score, the expression of Beclin1, LC3B-Ⅱ/Ⅰ and LC3B-Ⅱin the CA1 region of hippocampus were increased (P<0.05), the scores of horizontal and vertical motion of the open-field test, the consumption of sucrose solution and the expression of PI3K, p-Akt and p-mTOR were decreased in the model group (P<0.05). After intervention, compared with the model group and the non-meridian-non-acupoint group, the Zea Longa neurological behavioral score, the expression of Beclin1, LC3B-Ⅱ/Ⅰ and LC3B-Ⅱin the CA1 region of hippocampus were decreased (P<0.05), the scores of horizontal and vertical motion of the open-field test, the consumption of sucrose solution and the expression of PI3K, p-Akt and p-mTOR were increased in the Tongdu Tiaoshen group (P<0.05). Tongdu Tiaoshen acupuncture can effectively improve the depression-like behavior in PSD rats, its mechanism may relate to the activation of PI3K/Akt/mTOR signaling pathway and the inhibition of hippocampal neuron autophagy.

The Development of Pathological Dependence after Intermittent Use of Sodium Glutamate, but Not Sucrose or Sodium Chloride Solutions

The possibility of development of dependence was studied during the intermittent consumption of sucrose, sodium chloride, and sodium glutamate solutions. Rats were allowed to choose and consume solutions of sucrose, sodium chloride, and sodium glutamate for 28 days. On days 29-31 of the experiment, the animals were deprived of the preferred solutions. On days 32-33, the solutions of sucrose, sodium chloride, and sodium glutamate, but not water were provided again. The consumption of sucrose and sodium chloride solutions did not increase, but consumption of 0.5 and 1% sodium glutamate solutions increased after 3-days withdrawal. The consumption of 2% solution of sodium glutamate was the same before and after withdrawal. The observed effects of sodium glutamate deprivation probably indicate the development of pathological glutamate dependence.

Effect of short-term intake of high- and low-concentrations of sucrose solution on the neurochemistry of male and female mice.

The effect of short-term intake of high- and low-concentrations of sucrose solution on the neurochemistry of male and female mice was studied. The body weight, feed intake, sucrose solution consumption and brain monoamine neurotransmitters were determined after 34 days' intake of 1% and 8% sucrose solutions. The gene expression and protein levels related to dopamine and opioids were also determined. The results showed that the intake of 1% and 8% sucrose solution for 34 days did not cause significant changes in the weight development of both male and female mice. The preference for sucrose varies with sex. Both males and females had greater preference for the high concentration sucrose solution than the low concentration sucrose solution. The continuous intake of sucrose stimulated the release of monoamine neurotransmitters (DA, 5-HT, NE) in the brains of mice, and the reward effect of 8% sucrose solution is significantly higher than that of 1% sucrose solution. The sex of mice did not affect the release of neurotransmitters. The gene expressions of D1 and D2 were up-regulated in the 1% sucrose group of male mice, while the OPRM1 gene expression was down-regulated. The expression of these three genes in the 8% sucrose group of male mice was all down-regulated, while the gene expressions of D1 and D2 in the 1% and 8% sucrose group (p < 0.05) of female mice were both up-regulated.

Long-term sucrose solution consumption causes metabolic alterations and affects hepatic oxidative stress in Wistar rats.

ABSTRACTAs the number of overweight and obese people has risen in recent years, there has been a parallel increase in the number of people with metabolic syndrome, diabetes and non-alcoholic fatty liver disease. The consumption of artificially sweetened beverages contributes to these epidemics. This study investigated the long-term effects of ingestion of a 40% sucrose solution on serum and hepatic parameters in male Wistar rats (Rattus norvegicus). After 180 days, the glycemic response, lipid profile and hepatic oxidative stress were compared to those of rats maintained on water. Sucrose ingestion led to higher body weight, increased fat deposits, reduced voluntary food intake and reduced feeding efficiency. Rats that received sucrose solution showed early signs of glucose intolerance and insulin resistance, such as hyperinsulinemia. Serum triacylglycerol (TG), very-low density lipoprotein (VLDL), cholesterol, ALT and AST levels increased after sucrose consumption. Elevated malondialdehyde and superoxide dismutase (SOD) levels and reduced glutathione levels characterize the hepatic oxidative stress due to sucrose ingestion. Liver sample histology showed vacuolar traces and increased fibrotic tissue. Our data showed the harmful effects of chronic consumption of sucrose solution, which can cause alterations that are found frequently in obesity, glucose intolerance and non-alcoholic hepatic disease, characteristics of metabolic syndrome.

Antidepressant Effects and Mechanisms of the Total Iridoids of Valeriana jatamansi on the Brain-Gut Axis.

Valeriana jatamansi is widely used in Chinese folk medicine and contains iridoids as important active ingredients. The brain-gut axis describes a complex bidirectional system between the central nervous system and the gastrointestinal tract. Herein, we evaluated the antidepressant effects of total iridoids of Valeriana jatamansi (TIV) and preliminarily investigated the effects of gut microbiota on their antidepressant effects using a chronic, unpredictable mild-stress mouse model. Mice were given 5.7, 11.4, or 22.9 mg/kg TIV for 1 week. Fluoxetine (2.6 mg/kg) served as a positive control. Body weight was measured, and behavioral tests including SPT and TST were applied. Colon pathology was assessed through hematoxylin-eosin staining. Additionally, levels of serotonin (5-hydroxytryptamine, 5-HT), norepinephrine (NE), substance P (SP) and corticotropin-releasing factor (CRF) in the hippocampus and colon were measured by ELISA. In addition, 16SrRNA gene sequencing was performed to explore changes in intestinal microbiota richness and diversity. Our results demonstrated that the model group showed significant depression-like behavior, while the fluoxetine group showed improved depression-like symptoms; after administration, TIV increased body weight, sucrose solution consumption, and ameliorated depression-like behaviors. The overall cell degeneration in colons also improved. In addition, TIV modulated the levels of 5-HT, NE, SP, and CRF expression in the hippocampus and colon. The diversity and richness of gut microbes increased compared to the model group. We therefore conclude that the antidepressant effects of TIV may be related to gut flora structures and regulation of 5-HT, NE, SP, and CRF in the brain and intestine.

Manipulations of Central Amygdala Neurotensin Neurons Alter the Consumption of Ethanol and Sweet Fluids in Mice.

The central nucleus of the amygdala plays a significant role in alcohol use and other affective disorders; however, the genetically-defined neuronal subtypes and projections that govern these behaviors are not well known. Here we show that neurotensin neurons in the central nucleus of the amygdala of male mice are activated by in vivo ethanol consumption and that genetic ablation of these neurons decreases ethanol consumption and preference in non-ethanol-dependent animals. This ablation did not impact preference for sucrose, saccharin, or quinine. We found that the most robust projection of the central amygdala neurotensin neurons was to the parabrachial nucleus, a brain region known to be important in feeding behaviors, conditioned taste aversion, and alarm. Optogenetic stimulation of projections from these neurons to the parabrachial nucleus is reinforcing, and increases ethanol drinking as well as consumption of sucrose and saccharin solutions. These data suggest that this central amygdala to parabrachial nucleus projection influences the expression of reward-related phenotypes and is a novel circuit promoting consumption of ethanol and palatable fluids.SIGNIFICANCE STATEMENT Alcohol use disorder (AUD) is a major health burden worldwide. Although ethanol consumption is required for the development of AUD, much remains unknown regarding the underlying neural circuits that govern initial ethanol intake. Here we show that ablation of a population of neurotensin-expressing neurons in the central amygdala decreases intake of and preference for ethanol in non-dependent animals, whereas the projection of these neurons to the parabrachial nucleus promotes consumption of ethanol as well as other palatable fluids.

Steroid receptor RNA activator affects the development of poststroke depression by regulating the peroxisome proliferator-activated receptor γ signaling pathway.

The long noncoding RNA, steroid receptor RNA activator (SRA), has been reported to be involved in the development of many types of disease in humans. The aim of this study was to evaluate whether SRA was associated with poststroke depression (PSD). A PSD rat model was established, and depression-like behaviors and sucrose consumption in rats with PSD were analyzed. Reverse transcription-quantitative PCR (RT-PCR), western blot and luciferase dual reporter assay analyses were performed to detect the expression of peroxisome proliferator-activated receptor γ (PPARγ) expression following SRA small interfering RNA (siRNA) treatment. Compared with the control, the horizontal and vertical movement scores and consumption of sucrose solution were decreased in the PSD, PSD + LV-SRA and PSD + pioglitazone groups at 7 days post-SRA-siRNA treatment, while they were increased in the PSD + LV-SRA and PSD + pioglitazone groups. Furthermore, SRA expression in the PSD, PSD + LV-SRA and PSD + pioglitazone groups was lowered compared with the control group at 7 days postinjection. SRA increased the reported luciferase activity, but pioglitazone had no effect on the luciferase activity induced by SRA. SRA upregulated PPARγ mRNA and protein expression, whereas SRA siRNA significantly downregulated its expression. No significant differences in characteristics were identified between rats with and without PSD. SRA was more highly expressed in rats with PSD than rats without PSD. Collectively, this study suggests that SRA is associated with PSD through PPARγ signaling, indicating a potential therapeutic target of SRA for controlling PSD.