scholarly journals Changes in serum cholinesterase (EC 3 1 * 1 * 8) activity in rats consuming a high-fat diet

1989 ◽  
Vol 62 (2) ◽  
pp. 343-348 ◽  
Author(s):  
Jesus Osada ◽  
Hortensia Aylagas ◽  
Gonzalo Cao ◽  
Maria Jesus MIRo−Obradors ◽  
Evangelina Palacios−Alaiz

Adult male rats were fed on a control diet containing (g/kg) carbohydrate 600, lipid 35 and protein 190, or on a high-fat diet containing carbohydrate 360, lipid 420 and protein 120. After 30 d, the high-fat diet provoked a decrease in serum cholinesterase (EC3.1.1.8) activity which was reversed by feeding rats on the control diet. The observed decrease after 90 d on the high-fat diet was not seen if a simultaneous daily intraperitoneal injection of a lipotrophic agent containing (mg/kg) S-adenosyl-l-methionine 3, coenzyme A 0.1, UDP-glucose 30 and CDP-choline 1.5 was given to rats on the high-fat diet. The findings are discussed in relation to the apparent susceptibility of serum cholinesterase to dietary components and its possible role in lipid metabolism.

2020 ◽  
Vol 8 (6) ◽  
pp. 860 ◽  
Author(s):  
Yinzhao Zhong ◽  
Bo Song ◽  
Changbing Zheng ◽  
Shiyu Zhang ◽  
Zhaoming Yan ◽  
...  

Here, we investigated the roles and mechanisms of flavonoids from mulberry leaves (FML) on lipid metabolism in high fat diet (HFD)-fed mice. ICR mice were fed either a control diet (Con) or HFD with or without FML (240 mg/kg/day) by oral gavage for six weeks. FML administration improved lipid accumulation, alleviated liver steatosis and the whitening of brown adipose tissue, and improved gut microbiota composition in HFD-fed mice. Microbiota transplantation from FML-treated mice alleviated HFD-induced lipid metabolic disorders. Moreover, FML administration restored the production of acetic acid in HFD-fed mice. Correlation analysis identified a significant correlation between the relative abundances of Bacteroidetes and the production of acetic acid, and between the production of acetic acid and the weight of selected adipose tissues. Overall, our results demonstrated that in HFD-fed mice, the lipid metabolism improvement induced by FML administration might be mediated by gut microbiota, especially Bacteroidetes-triggered acetic acid production.


Foods ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2202
Author(s):  
Micaelle Oliveira de Luna Freire ◽  
Luciana Caroline Paulino do Nascimento ◽  
Kataryne Árabe Rimá de Oliveira ◽  
Alisson Macário de Oliveira ◽  
Thiago Henrique Napoleão ◽  
...  

High-fat diet (HFD) consumption has been linked to dyslipidemia, low-grade inflammation and oxidative stress. This study investigated the effects of a mixed formulation with Limosilactobacillusfermentum 139, L. fermentum 263 and L. fermentum 296 on cardiometabolic parameters, fecal short-chain fatty acid (SCFA) contents and biomarkers of inflammation and oxidative stress in colon and heart tissues of male rats fed an HFD. Male Wistar rats were grouped into control diet (CTL, n = 6), HFD (n = 6) and HFD with L. fermentum formulation (HFD-Lf, n = 6) groups. The L.fermentum formulation (1 × 109 CFU/mL of each strain) was administered twice a day for 4 weeks. After a 4-week follow-up, biochemical parameters, fecal SCFA, cytokines and oxidative stress variables were evaluated. HFD consumption caused hyperlipidemia, hyperglycemia, low-grade inflammation, reduced fecal acetate and propionate contents and increased biomarkers of oxidative stress in colon and heart tissues when compared to the CTL group. Rats receiving the L. fermentum formulation had reduced hyperlipidemia and hyperglycemia, but similar SCFA contents in comparison with the HFD group (p < 0.05). Rats receiving the L. fermentum formulation had increased antioxidant capacity throughout the colon and heart tissues when compared with the control group. Administration of a mixed L. fermentum formulation prevented hyperlipidemia, inflammation and oxidative stress in colon and heart tissues induced by HFD consumption.


2021 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Abimbola Abiodun Adeyemi-Doro ◽  
Sule Ola Salawu ◽  
Akintunde Afolabi Akindahunsi

Purpose The purpose of this study is to assess the effects of two green leafy vegetables (Gongronema latifolium and Celosia argentea) on the hepatic biomarkers [Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST)], cardiac biomarkers [Creatine Kinase (CK) and Lactate Dehydrogenase (LDH)] and histopathology of the heart of high-fat diet-induced hyperlipidemic rats, with the aim of evaluating the vegetables as functional foods. Design/methodology/approach Experimental diets consisted of Control Diet (CD), High-Fat Diet (HFD), High-Fat Diet with Blanched Celosia argentea (HCB), High-Fat Diet with Unblanched Celosia argentea (HCU), High-Fat diet with Blanched Gongronema latifolium (HGB) and High-Fat Diet with Unblanched Gongronema latifolium (HGU). Seventy-five albino male rats (weighing 180–200 g) were used. The animals were divided into 15 groups of five albino rats each. Animals in Groups 1, 2 and 3 were fed with CD, HFD only and HFD with Atorvastin (5 mg/kg b.w), respectively. Animals in Groups 4, 5 and 6 were fed with 5, 10 and 15% HCB, respectively. Animals in Groups 7, 8 and 9 were fed with 5, 10 and 15% HCU, respectively, whereas animals in Groups 10, 11 and 12 were fed with 5, 10 and 15% HGB, respectively, and animals in Groups 13, 14 and 15 were fed with 5, 10 and 15% diet-inclusion of HGU, respectively. Findings The incorporation of the vegetal matter into the diet brought about a significant reduction (p = 0.05) in the activities of ALT, AST, CK and LDH when compared with HFD. However, the histological examination showed no pathological lesion, only at 15% inclusion of the vegetables. Originality/value The paper established that the incorporation of Celosia argentea and Gongronema latifolium into diet, most especially at 15% inclusion, may serve as functional food in the management of hyperlipidemia and associated complications.


2009 ◽  
Vol 21 (9) ◽  
pp. 110
Author(s):  
X. Yang ◽  
K. R. Dunning ◽  
T. E. Hickey ◽  
R. J. Norman ◽  
X. Liang ◽  
...  

Intracellular neutral lipids are stored in discrete droplets that are surrounded by lipid associated proteins, such as adipophilin and perilipin, which control cellular lipid metabolism by regulating the access of lipases. The role of lipids in oocyte maturation is unclear, although they have a potential role as an energy source for the oocyte and early embryo. To elucidate potential mechanisms controlling lipid utilisation in the peri-ovulatory cumulus-oocyte-complex (COC) we 1) localised lipid droplets by immunohistochemistry for adipophilin and perilipin and direct staining of neutral lipids with BODIPY and 2) investigated whether a high fat diet can alter oocyte lipid quantity or localisation. Ovaries were isolated from 21 day old mice before and 10h after the ovulation stimulus hCG. Adipophilin and perilipin were both detected by immunohistochemistry in peri-ovulatory follicles with similar localisation before and after hCG. In separate experiments, adult mice were fed a high fat or control diet for 4 weeks and COCs were isolated from preovulatory follicles prior to hCG or from the oviduct 13h after hCG stimulation followed by BODIPY staining and quantification with confocal microscopy. BODIPY staining showed that COCs possess low levels of lipids evenly distributed in the oocyte before hCG but increased lipid assembled as droplets in the oocyte after ovulation. In mice fed a high fat diet, intracellular lipids were markedly increased in both the cumulus cells and oocytes from preovulatory and ovulated COCs. The ubiquitous expression of lipid droplet proteins in the peri-ovulatory follicle together with the changes in neutral lipid storage concurrent with ovulation suggests that lipid metabolism play an important role in oocyte release, transport and/or developmental competence. Furthermore, the dramatic effect of dietary fat on COC lipid content may contribute to the impaired oocyte quality we have observed in obese mice as well as reduced fertility in obese women


Author(s):  
María J. Ríos-Lugo ◽  
Vanesa Jiménez-Ortega ◽  
Pilar Cano-Barquilla ◽  
Pilar Fernández Mateos ◽  
Eduardo J. Spinedi ◽  
...  

AbstractPrevious studies indicate that the administration of melatonin caused body weight and abdominal visceral fat reductions in rodent models of hyperadiposity. The objective of the present study performed in high-fat fed rats was to evaluate the activity of melatonin on gene expression of some medial basal hypothalamus (MBH) signals involved in feeding behavior regulation, including neuropeptide Y (NPY), proopiomelanocortin (POMC), prolactin-releasing peptide (PrRP), leptin- and insulin-receptors (R) and insulin-R substrate (IRS)-1 and -2. Blood levels of leptin and adiponectin were also measured.Adult Wistar male rats were divided into four groups (n=16 per group): (i) control diet (3% fat); (ii) high-fat (35%) diet; (iii) high-fat diet+melatonin; (iv) control diet+melatonin. Rats had free access to high-fat or control chow and one of the following drinking solutions: (a) tap water; (b) 25 μg/mL of melatonin.After 10 weeks, the high-fat fed rats showed augmented MBH mRNA levels of NPY, leptin-R, PrRP, insulin-R, IRS-1 and IRS-2. The concomitant administration of melatonin counteracted this increase. Feeding of rats with a high-fat diet augmented expression of the MBH POMC gene through an effect insensitive to melatonin treatment. The augmented levels of circulating leptin and adiponectin seen in high-fat fed rats were counteracted by melatonin as was the augmented body weight: melatonin significantly attenuated a body weight increase in high-fat fed rats without affecting chow or water consumption. Melatonin augmented plasma leptin and adiponectin in control rats.The results indicate that an effect on gene expression of feeding behavior signals at the central nervous system (CNS) may complement a peripheral rise of the energy expenditure produced by melatonin to decrease body weight in high-fat fed rats.


2021 ◽  
Author(s):  
Ayumi Eguchi ◽  
Sayaka Mizukami ◽  
Misato Nakamura ◽  
Sousuke Masuda ◽  
Hirotada Murayama ◽  
...  

Abstract Nonalcoholic fatty liver disease is a hepatic disorder with deposition of fat droplets, and has a high risk of progression to steatosis-related hepatitis and irreversible hepatic cancer. Metronidazole (MNZ) is an antiprotozoal and antimicrobial agent widely used to treat patients infected with anaerobic bacteria and intestinal parasites; however, MNZ has also been shown to induce liver tumors in rodents. To investigate the effects of MNZ on steatosis-related early-stage hepatocarcinogenesis, male rats treated with N-nitrosodiethylamine following 2/3 hepatectomy at week 3 were received a control basal diet, high fat diet (HFD), or HFD containing 0.5% MNZ. The HFD induced obesity and steatosis in liver, accompanied by altered expression of Pparg and Fasn, genes related to lipid metabolism. MNZ increased nuclear translocation of lipid metabolism-related transcription factor peroxisome proliferator-activated receptor gamma in hepatocytes, together with altered liver expression of lipid metabolism genes (Srebf1, Srebf2, Pnpla2). Furthermore, MNZ significantly increased the number of preneoplastic liver foci, accompanied by DNA double-strand breaks and late-stage autophagy inhibition, as reflected by increased levels of γ-H2AX, LC3, and p62. Therefore, MNZ could induce steatosis-related hepatocarcinogenesis by inducing DNA double-strand breaks and modulating autophagy in HFD-fed rats.


2014 ◽  
Vol 307 (6) ◽  
pp. G642-G654 ◽  
Author(s):  
Amy M. Garcia ◽  
Derek Wakeman ◽  
Jianyun Lu ◽  
Christopher Rowley ◽  
Taylor Geisman ◽  
...  

Effective therapies are limited for patients with parenteral nutrition-dependent short bowel syndrome. We previously showed that intestinal expression of the transcriptional coregulator tetradecanoyl phorbol acetate-induced sequence 7 ( tis7) is markedly increased during the adaptive response following massive small bowel resection and tis7 plays a role in normal gut lipid metabolism. Here, we further explore the functional implications of tis7 deletion in intestinal lipid metabolism and the adaptive response following small bowel resection. Intestinal tis7 transgenic ( tis7tg), tis7−/−, and wild-type (WT) littermates were subjected to 50% small bowel resection. Mice were fed a control or a high-saturated-fat (42% energy) diet for 21 days. Survival, body weight recovery, lipid absorption, mucosal lipid analysis, and the morphometric adaptive response were analyzed. Quantitative real-time PCR was performed to identify tis7 downstream gene targets. Postresection survival was markedly reduced in high-fat, but not control, diet-fed tis7−/− mice. Decreased survival was associated with anastomotic inflammation and intestinal obstruction postresection. High-fat, but not control, diet-fed tis7−/− mice had increased intestinal IL-6 expression. Intestinal lipid trafficking was altered in tis7−/− compared with WT mice postresection. In contrast, high-fat diet-fed tis7tg mice had improved survival postresection compared with WT littermates. High-fat diet feeding in the setting of tis7 deletion resulted in postresection anastomotic inflammation and small bowel obstruction. Tolerance of a calorie-rich, high-fat diet postresection may require tis7 and its target genes. The presence of luminal fat in the setting of tis7 deletion promotes an intestinal inflammatory response postresection.


2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Manisha Ganeshan ◽  
Pothaganti B. Sainath ◽  
Inagadapa J. Naga Padmavathi ◽  
Lagishetty Venu ◽  
Yedla Durga Kishore ◽  
...  

Growthin uterois largely a reflection of nutrient and oxygen supply to the foetus. We studied the effects of Mn restrictionper se, maternal Mn restriction, and postnatal high-fat feeding in modulating body composition, lipid metabolism and adipocyte function in Wistar/NIN (WNIN) rat offspring. Female weanling, WNIN rats receivedad libitumfor 4 months, a control or Mn-restricted diet and were mated with control males. Some restricted mothers were rehabilitated with control diet from conception (MnRC) or parturition (MnRP), and their offspring were raised on control diet. Some restricted offspring were weaned onto control diet (MnRW), while others continued on restricted diet throughout (MnR). A set of offspring from each group was fed high-fat diet from 9 months onwards. Body composition, adipocytes function, and lipid metabolism were monitored in male rat offspring at regular intervals. Maternal manganese restriction increased the susceptibility of the offspring to high-fat-induced adiposity, dyslipidaemia, and a proinflammatory state but did not affect their glycemic or insulin status.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Hongyu Zhang ◽  
Chengguang Song ◽  
Rong Yan ◽  
Hongbo Cai ◽  
Yi Zhou ◽  
...  

Abstract Background Low dose of NP exposure can alter adipose tissue formation, and the intake of high-fat diet (HFD) can also lead to the fatty liver disease. We investigated the combined effect of NP and HFD on the first offspring of rats, and whether this effect can be passed to the next generation and the possible mechanisms involved. Methods Pregnant rats had access to be treated with 5 μg/kg/day NP and normal diet. The first generation rats were given normal diet and HFD on postnatal day 21, respectively. Then the second generation rats started to only receive normal diet without NP or HFD. Body weight, organ coefficient of liver tissues, lipid profile, biochemical indexes and the expression of genes involved in lipid metabolism, as well as liver histopathology were investigated in male offspring of rats. Results NP and HFD interaction had significant effect on the birth weight, body weight and liver tissue organ coefficient of first generation male rats. And HFD aggravated abnormal lipid metabolism, even abnormal liver function and liver histopathological damage of first generation male rats produced by the NP. And this effect can be passed on to the second generation rats. HFD also accelerated the mRNA level of fatty acid synthesis genes such as Lpl, Fas, Srebp-1 and Ppar-γ of first generation rats induced by perinatal exposure to NP, even passed on to the second generation of male rats. NP and HFD resulted in synergistical decrease of the protein expression level of ERα in liver tissue in F2 male rats. Conclusion HFD and NP synergistically accelerated synthesis of fatty acids in liver of male offspring rats through reducing the expression of ERα, which induced abnormal lipid metabolism, abnormal liver function and hepatic steatosis. Moreover, all of these damage passed on to the next generation rats.


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