Imazalil resulted in glucolipid metabolism disturbance and abnormal m6A RNA methylation in the liver of dam and offspring mice.

As a fungicide with the characteristics of high effectiveness, internal absorption and broad spectrum, imazalil is widely used to prevent and treat in fruits and vegetables. Here, pregnant C57BL/6 mice were exposed to imazalil at dietary levels of 0, 0.025‰, and 0.25‰ through drinking water during pregnancy and lactation. We then analyzed the phenotype, metabolome, and expression of related genes and proteins in the livers of mice. There was a marked decrease in the body and liver weights of male offspring mice after maternal imazalil exposure, while this effect on the dam and female offspring was slight. Metabolomics analyses revealed that imazalil significantly altered the metabolite composition of liver samples from both dams and offspring. The preliminary results of the analysis indicated that glucolipid metabolism was the pathway most significantly affected by imazalil. We performed a coabundance association analysis of metabolites with significant changes in the pathway of glycolipid metabolism, and IMZ altered the networks of both dams and offspring compared with the network in control mice, especially in male offspring. The hepatic triglyceride, non-esterified fatty acid and glucose levels were increased significantly in the dams but decreased significantly in male offspring after maternal imazalil exposure. Furthermore, the expression levels of genes associated with glycolipid metabolism and m6A RNA methylation were significantly affected by maternal intake of imazalil. Imazalil-induced glucolipid metabolism disturbance was highly correlated with m6A RNA methylation. In conclusion, maternal imazalil exposure resulted in glucolipid metabolism disturbance and abnormal m6A RNA methylation in the livers of dams and offspring mice. We expected that the information acquired in this study will provide novel evidence for understanding the effect of maternal imazalil exposure on potential health risks.

Impacts of prothioconazole and prothioconazole-desthio on bile acid and glucolipid metabolism: Upregulation of CYP7A1 expression in HepG2 cells.

As an efficient triazole fungicide, prothioconazole (PTC) is widely used for the prevention and control of plant fungal pathogens. It was reported that the residues of PTC and prothioconazole-desthio (PTC-d) have been detected in the environment and crops, and the effects of PTC-d may be higher than that of PTC. Currently, PTC and PTC-d have been proven to induce hepatic metabolic disorders. However, their toxic effects on cellular bile acid (BA) and glucolipid metabolism remain unknown. In this study, HepG2 cells were exposed to 1-500 µM of PTC or PTC-d. High concentrations of PTC and PTC-d were found to induce cytotoxicity; thus, subsequent experimental exposure was conducted at concentrations of 10-50 µM. The expression levels of CYP7A1 and TG synthesis-related genes and levels of TG and total BA were observed to increase in HepG2 cells. Molecular docking analysis revealed direct interactions between PTC or PTC-d and CYP7A1 protein. To further investigate the underlying mechanisms, PTC and PTC-d were treated to HepG2 cells in which CYP7A1 expression was knocked down using siCYP7A1. It was observed that PTC and PTC-d affected the BA metabolism process and regulated the glycolipid metabolism process by promoting the expression of CYP7A1. In summary, we comprehensively analyzed the effects and mechanisms of PTC and PTC-d on cellular metabolism in HepG2 cells, providing theoretical data for evaluating the safety and potential risks associated with these substances.

Characteristics of glucolipid metabolism and oxidative stress in breeding pigeons (Columba livia) during lactation.

Breeding pigeons is a fundamental source of profit in various enterprises but little is known on the metabolic laws governing their lactation. In this study, we analysed the metabolic profile of different sex of breeding pigeons (Columba livia, European pigeons, Mimas) during lactation. We found that male pigeons exhibited catabolism during lactation. Extension of lactation resulted in increased weight loss, then slow recovery of body weight. Conversely, the weight loss in female pigeons peaked on the seventh day of lactation. They then gradually recovered their body weight. Male pigeons showed more duration of combing, while female pigeons showed more duration of resting. In male pigeons, except for triglyceride (TG), which increased, blood lipid indexes barely changed during lactation. Conversely, in females, both TG and total cholesterol increased in middle and late lactation. The level of oxidative stress in female pigeons during lactation was higher than in males, lipid peroxide malondialdehyde, hydrogen peroxide (H2 O2 ), plasma calcium (Ca) and phosphorus (P) levels increased in late lactation. Levels of estradiol and progesterone in female pigeons increased during lactation, whereas those of luteotropic hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL) and testosterone gradually decreased. As per LC-MS spectra analysis, the differential metabolites in the plasma on the day of hatching and before laying in female pigeons in lactation were enriched in retrograde endocannabinoid signalling, α-linolenic acid, arachidonic acid, choline, glycerophospholipid metabolisms, and valine, leucine, and isoleucine degradations. Levels of fatty acids, amino acids, sphingomyelin and phosphatidylinositol related to the secretion of pigeon milk had reduced, whereas the levels of phosphatidylcholine, phosphatidylethanolamine, and TG, which are all related to egg production, had increased. In conclusion, our study systematically revealed the different metabolic characteristics of male and female breeding pigeons during lactation. This is useful for precision feeding of pigeons and applicable in nutritional interventions for improved production.

LncRNA Tug1 relieves the steatosis of SelenoF-knockout hepatocytes via sponging miR-1934-3p.

Metabolic dysfunction associated with fatty liver disease (MAFLD), always accompanied by disturbance of glucose and lipid metabolism, is becoming the most difficult obstacle in the next decades. In the current research, we uncover that the potent non-coding RNA Tug1, which is related to metabolic enzymes, regulates hepatocytes steatosis induced by sodium palmitate via miR-1934-3p absorbing. The knockdown of lncRNA-Tug1 distinctly rescues the increased expression level of glycolytic enzymes and fatty acid synthetase via releasing more mature miR-1934-3p in hepatocytes. Moreover, miR-1934-3p suppresses Selenoprotein F (SelenoF) through binding with the SelenoF 3'UTR effectors; importantly, we demonstrated that the deletion of SelenoF consistent with the lncRNA-Tug1's effecting on metabolism enzymes. In the current paper, the interaction of Tug1/miR-1934-3p/SelenoF was verified by the dual-luciferase reporter system, and IRS1/AKT pathway possesses the essential role in glucolipid metabolism when SelenoF is deleted. We concluded that lncRNA Tug1 functioned as ceRNA to alleviate steatosis and glycolysis in hepatocytes of C57BL/6 through adsorbing miR-1934-3p to release SelenoF and triggering IRS/AKT pathway. The Tug1/miR-1934-3p/SelenoF constructed the ceRNA interact network Selenoprotein F accelerates glucolipid metabolism via IRS1/AKT pathway SelenoF-/- alleviates steatosis in mice liver.

The relationship between gut microbiota, short-chain fatty acids, and glucolipid metabolism in pregnant women with large for gestational age infants.

AIM: To elucidate the association between gut microbiota, short-chain fatty acids (SCFAs), and glucolipid metabolism in women with large for gestational age (LGA) infants. METHODS AND RESULTS: A single-center, observational prospective cohort study was performed at a tertiary hospital in Wenzhou, China. Normal pregnant women were divided into LGA group and appropriate for gestational age (AGA) group according to the neonatal birth weight. Fecal samples were collected from each subject before delivery for the analysis of gut microbiota composition (GMC) and SCFAs. Blood samples were obtained at 24-28 weeks of gestation age to measure fasting blood glucose and fasting insulin levels, as well as just before delivery to assess serum triglycerides, total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein. The GMC exhibited differences at various taxonomic levels. Within the Firmicutes phylum, genus Lactobacillus, genus Clostridium, species Lactobacillus agil, and species Lactobacillus salivarius were enriched in the LGA group. Microbispora at genus level, Microbispora rosea at species level belonging to the Actinobacteria phylum, Neisseriales at order level, Bartonellaceae at family level, Paracoccus aminovorans, and Methylobacterium at genus level from the Proteobacteria phylum were more abundant in the LGA group. In contrast, within the Bacteroidetes phylum, Prevotella at genus level and Parabacteroides distasonis at species level were enriched in the AGA group. Although there were few differences observed in SCFA levels and most glucolipid metabolism indicators between the two groups, the serum HDL level was significantly lower in the LGA group compared to the AGA group. No significant relevance among GMC, SCFAs, and glucolipid metabolism indicators was found in the LGA group or in the AGA group. CONCLUSIONS: Multiple different taxa, especially phylum Firmicutes, genus Prevotella, and genus Clostridium, might play an important role in excessive fetal growth, and LGA might be associated with the lower serum HDL level.

Characteristics of glucolipid metabolism and complications in novel cluster-based diabetes subgroups: a retrospective study.

BACKGROUND: Glucolipid metabolism plays an important role in the occurrence and development of diabetes mellitus. However, there is limited research on the characteristics of glucolipid metabolism and complications in different subgroups of newly diagnosed diabetes. This study aimed to investigate the characteristics of glucolipid metabolism and complications in novel cluster-based diabetes subgroups and explore the contributions of different glucolipid metabolism indicators to the occurrence of complications and pancreatic function. METHODS: This retrospective study included 547 newly diagnosed type 2 diabetes patients. Age, body mass index (BMI), glycated hemoglobin (HbA1C), homeostasis model assessment-2 beta-cell function (HOMA2-ß), and homeostasis model assessment-2 insulin resistance (HOMA2-IR) were used as clustering variables. The participants were divided into 4 groups by k-means cluster analysis. The characteristics of glucolipid indicators and complications in each subgroup were analyzed. Regression analyses were used to evaluate the impact of glucolipid metabolism indicators on complications and pancreatic function. RESULTS: Total cholesterol (TC), triglycerides (TG), triglyceride glucose index (TyG), HbA1C, fasting plasma glucose (FPG), and 2-h postprandial plasma glucose (2hPG) were higher in the severe insulin-resistant diabetes (SIRD) and severe insulin-deficient diabetes (SIDD) groups. Fasting insulin (FINS), fasting C-peptide (FCP), 2-h postprandial insulin (2hINS), 2-h postprandial C-peptide (2hCP), and the monocyte-to-high-density lipoprotein cholesterol ratio (MHR) were higher in mild obesity-related diabetes (MOD) and SIRD. 2hCP, FCP, and FINS were positively correlated with HOMA2-ß, while FPG, TyG, HbA1C, and TG were negatively correlated with HOMA2-ß. FINS, FPG, FCP, and HbA1C were positively correlated with HOMA2-IR, while high-density lipoprotein (HDL) was negatively correlated with HOMA2-IR. FINS (odds ratio (OR),1.043;95% confidence interval (CI) 1.006 ~ 1.081), FCP (OR,2.881;95%CI 2.041 ~ 4.066), and TyG (OR,1.649;95%CI 1.292 ~ 2.104) contributed to increase the risk of nonalcoholic fatty liver disease (NAFLD); 2hINS (OR,1.015;95%CI 1.008 ~ 1.022) contributed to increase the risk of atherosclerotic cardiovascular disease (ASCVD); FCP (OR,1.297;95%CI 1.027 ~ 1.637) significantly increased the risk of chronic kidney disease (CKD). CONCLUSIONS: There were differences in the characteristics of glucolipid metabolism as well as complications among different subgroups of newly diagnosed type 2 diabetes. 2hCP, FCP, FINS, FPG, TyG, HbA1C, HDL and TG influenced the function of insulin. FINS, TyG, 2hINS, and FCP were associated with ASCVD, NAFLD, and CKD in newly diagnosed T2DM patients.

Berberine alleviates intestinal barrier dysfunction in glucolipid metabolism disorder hamsters by modulating gut microbiota and gut-microbiota-related tryptophan metabolites.

BACKGROUND: Barberry plants can be considered as useful additives and functional compounds in various industries, especially in the food industry. Berberine (BBR), the most important functional compound in the barberry roots, has recently been used to treat obesity, diabetes, and atherosclerosis. Gut microbiota and the intestinal barrier play an important role in the development of glucolipid metabolism disorders (GLMDs). However, the association of gut microbiota metabolism disorder and the intestinal barrier dysfunction effect of BBR in GLMDs remains elusive. RESULTS: The results showed that administration of BBR could increase the number of colonic glands and goblet cell mucus secretion, improve the intestinal barrier function, and reduce the serum glycolipid level in GLMD hamsters. Interestingly, BBR was metabolized into 12 metabolites by gut microbiota, and the main metabolic pathways were oxidation, demethylation, and hydrogenation. In addition, BBR significantly improved the species diversity and uniformity of gut microbiota and promoted the proliferation of beneficial microbiota. Furthermore, the levels of tryptophan metabolites, such as indole, indole-3-acetamide, indole-3-acetaldehyde, indole-3-pyruvic acid, and indole-3-acetic acid were significantly altered by BBR. Both the intestinal tight junction proteins and intestinal immune factors were altered by BBR. CONCLUSION: BBR could alleviate intestinal barrier dysfunction of GLMDs by modulating gut microbiota and gut-microbiota-related tryptophan metabolites, which may be one of the pharmacological mechanisms for the treatment of GLMDs. © 2022 Society of Chemical Industry.

Dietary soybean lecithin promoted growth performance and feeding in juvenile Chinese perch (Siniperca chuatsi) could be by optimizing glucolipid metabolism.

To explore the potential benefits of dietary phospholipids (PLs) in fish glucose metabolism and to promote feed culture of Chinese perch (Siniperca chuatsi), we set up six diets to feed Chinese perch (initial mean body weight 37.01 ± 0.20 g) for 86 days, including: Control diet (CT), 1% (SL1), 2% (SL2), 3% (SL3), 4% (SL4) soybean lecithin (SL) and 2% (KO2) krill oil (KO) supplemental diets (in triplicate, 20 fish each). Our study found that the SL2 significantly improved the weight gain rate and special growth rate, but the KO2 did not. In addition, the SL2 diet significantly improved feed intake, which is consistent with the mRNA levels of appetite-related genes (npy, agrp, leptin A). Additionally, in the CT and SL-added groups, leptin A expression levels were nearly synchronized with serum glucose levels. Besides, the SL2 significantly upregulated expression levels of glut2, gk, cs, fas and downregulated g6pase in the liver, suggesting that it may enhance glucose uptake, aerobic oxidation, and conversion to fatty acids. The SL2 also maintained the hepatic crude lipid content unchanged compared to the CT, possibly by significantly down-regulating the mRNA level of hepatic lipase gene (hl), and by elevating serum low-density lipoprotein (LDL) level and intraperitoneal fat ratio in significance. Moreover, the serum high-density lipoprotein levels were significantly increased by PL supplementation, and the SL2 further significantly increased serum total cholesterol and LDL levels, suggesting that dietary PLs promote lipid absorption and transport. Furthermore, dietary SL at 1% level could enhance non-specific immune capacity, with serum total protein level being markedly higher than that in the CT group. In conclusion, it is speculated that the promotion of glucose utilization and appetite by 2% dietary SL could be linked. We suggest a 1.91% supplementation of SL in the diet for the best growth performance in juvenile Chinese perch.

Sex-dependent obesogenic effect of tetracycline on Drosophila melanogaster deteriorated by dysrhythmia.

Antibiotics have been identified as obesogens contributing to the prevalence of obesity. Moreover, their environmental toxicity shows sex dependence, which might also explain the sex-dependent obesity observed. Yet, the direct evidence for such a connection and the underlying mechanisms remain to be explored. In this study, the effects of tetracycline, which is a representative antibiotic found in both environmental and food samples, on Drosophila melanogaster were studied with consideration of both sex and circadian rhythms (represented by the eclosion rhythm). Results showed that in morning-eclosed adults, tetracycline significantly stimulated the body weight of females (AM females) at 0.1, 1.0, 10.0 and 100.0 µg/L, while tetracycline only stimulated the body weight of males (AM males) at 1.0 µg/L. In the afternoon-eclosed adults, tetracycline significantly stimulated the body weight of females (PM females) at 0.1, 1.0 and 100.0 µg/L, while it showed more significant stimulation in males (PM males) at all concentrations. Notably, the stimulation levels were the greatest in PM males among all the adults. The results showed the clear sex dependence of the obesogenic effects, which was diminished by dysrhythmia. Further biochemical assays and clustering analysis suggested that the sex- and rhythm-dependent obesogenic effects resulted from the bias toward lipogenesis against lipolysis. Moreover, they were closely related to the preference for the energy storage forms of lactate and glucose and also to the presence of excessive insulin, with the involvement of glucolipid metabolism. Such relationships indicated potential bridges between the obesogenic effects of pollutants and other diseases, e.g., cancer and diabetes.

Sex discrepancy in establishing mouse visceral obesity model induced by high-fat diet. / é«˜è„‚é¥®é£Ÿè¯±å¯¼çš„å† è„è‚¥èƒ–å°é¼ æ¨¡åž‹å­˜åœ¨æ€§åˆ«å·®å¼‚.

OBJECTIVES: To establish a mouse visceral obesity model, and to investigate the effect of animal sex on this model. METHODS: Thirty-two 4-week-old BALB/c mice were randomly divided into female control group, female high-fat group, male control group and male high-fat group with 8 mice in each group.The control groups were given ordinary diet, and the high-fat groups were given high-fat diet. After 12 weeks of feeding, body weight, visceral fat, fasting blood glucose, glucose tolerance, blood lipid and metabolism-related hormone levels were measured, and the composition of gut microbiota of mice was analyzed by 16S rRNA sequencing. RESULTS: The high fat diet resulted in a significant increase of body weight and visceral fat content in male mice; the pathological results showed significantly increased fat area, accumulation of liver fat droplets, increased total cholesterol, fasting blood glucose, oral glucose tolerance and serum insulin levels (all P<0.05), as well as significant insulin resistance (P<0.01). However, the above changes were not significant in female mice. Compared with the control groups, there was an increase in the relative abundance of obesity-related gut microbiota in the model groups (such as Blautia), and the microbiota structure changed significantly, while the changes were less obvious in female mice. CONCLUSIONS: A visceral obesity mouse model has been stably established by feeding high-fat diet in BALB/c male mice, showing visceral fat accumulation, metabolic dysfunction and gut microbiota changes; while female mice are not sensitive in this obesity model.

[Zuogui Jiangtang Qinggan Formula improves glucolipid metabolism in type 2 diabetes mellitus complicated with non-alcoholic fatty liver disease by regulating FoxO1/MTP/APOB signaling pathway].

This study aimed to investigate the effect and mechanism of Zuogui Jiangtang Qinggan Formula(ZGJTQG) on the glucolipid metabolism of type 2 diabetes mellitus(T2DM) complicated with non-alcoholic fatty liver disease(NAFLD). NAFLD was induced by a high-fat diet(HFD) in MKR mice(T2DM mice), and a model of T2DM combined with NAFLD was established. Forty mice were randomly divided into a model group, a metformin group(0.067 g·kg~(-1)), and high-and low-dose ZGJTQG groups(29.64 and 14.82 g·kg~(-1)), with 10 mice in each group. Ten FVB mice of the same age were assigned to the normal group. Serum and liver tissue specimens were collected from mice except for those in the normal and model groups after four weeks of drug administration by gavage, and fasting blood glucose(FBG) and fasting insulin(FINS) levels were measured. The levels of total cholesterol(TC), triglyceride(TG), and low-density lipoprotein(LDL) were detected by the single reagent GPO-PAP method. Very low-density lipoprotein(VLDL) was detected by enzyme-linked immunosorbent assay(ELISA). Alanine aminotransferase(ALT) and aspartate ami-notransferase(AST) were determined by the Reitman-Frankel assay. The pathological changes in the liver were observed by hematoxylin-eosin(HE) staining and oil red O staining. Real-time fluorescence-based quantitative polymerase chain reaction(real-time PCR) and Western blot were adopted to detect the mRNA and protein expression of forkhead transcription factor O1(FoxO1), microsomal triglyceride transfer protein(MTP), and apolipoprotein B(APOB) in the liver. The results showed that high-dose ZGJTQG could signi-ficantly reduce the FBG and FINS levels(P<0.05, P<0.01), improve glucose tolerance and insulin resistance(P<0.05, P<0.01), alleviate the liver damage caused by HFD which was reflected in improving liver steatosis, and reduce the serum levels of TC, TG, LDL, VLDL, ALT, and AST(P<0.05, P<0.01) in T2DM mice combined with NAFLD. The findings also revealed that the mRNA and protein expression of FoxO1, MTP, and APOB in the liver was significantly down-regulated after the intervention of high-dose ZGJTQG(P<0.05, P<0.01). The above study showed that ZGJTQG could effectively improve glucolipid metabolism in T2DM combined with NAFLD, and the mechanism was closely related to the regulation of the FoxO1/MTP/APOB signaling pathway.

Molecular characterization of insulin receptor (IR) in oriental fruit moth, Grapholita molesta (Lepidoptera: Tortricidae), and elucidation of its regulatory roles in glucolipid homeostasis and metamorphosis through interaction with miR-982490.

As an intermediate molecule in the Insulin/Insulin-like growth factor signalling pathway (IIS), the insulin receptor (IR) plays vital roles linking nutritional signals to the downstream regulation of metabolic homeostasis, development, metamorphosis, reproduction and stress responses. In the present study, we describe the molecular characteristics of IR in the cosmopolitan fruit boring pest, Grapholita molesta, and its predicted posttranscription regulator miR-982490, and elucidate its regulatory roles in glucolipid homeostasis and metamorphosis. Phylogenetic and domain analyses indicate that lepidopteran IRs normally cluster within families, and that four main domains are conserved in GmIR and those of other Lepidoptera. Bio-informatic prediction, synchronic expression profile evaluation and dual luciferase reporter assays indicated negative regulation of GmIR by miR-982490. Injection of miR-982490 agomir into fifth instar larvae yielded effects similar to dsGmIR injection, resulting in enhanced levels of trehalose and triglyceride in haemolymph, and reduced pupation success and pupal weight, both of which could be rescued by co-injection of dsGmIR and miR-982490 antagomir. We infer that GmIR regulates glucolipid homeostasis and affects G. molesta metamorphosis via interactions with its posttranscriptional regulator miR-982490. This study expands our understanding of the regulatory network of IIS in insect nutritional homeostasis and development.

A study on serum pro-neurotensin (PNT), furin, and zinc alpha-2-glycoprotein (ZAG) levels in patients with acromegaly.

PURPOSE: Acromegaly caused by growth hormone cell adenoma is commonly associated with abnormal glucolipid metabolism, which may result from changes in adipocytokine secretion. This study aims to investigate serum adipokine levels, including pro-neurotensin (PNT), furin, and zinc alpha-2-glycoprotein (ZAG), in acromegalic patients and the correlation between the levels of these three adipokines and GH levels and glucolipid metabolism indices. METHODS: Sixty-eight acromegalic patients and 121 controls were included, and their clinical data were recorded from electronic medical record system. Serum PNT, furin and ZAG levels were measured by ELISA. RESULTS: Serum PNT levels in acromegalic patients were significantly higher than controls (66.60 ± 12.36 vs. 46.68 ± 20.54 pg/ml, P < 0.001), and acromegaly was an independent influencing factor of PNT levels (P < 0.001). Moreover, subjects with the highest tertile of PNT levels had a close correlation with acromegaly (OR = 22.200, 95% CI 7.156 ~ 68.875, P < 0.001), even in Model 1 adjusted for gender and age and Model 2 adjusted for gender, age and BMI. Additionally, serum PNT levels were positively correlated with BMI (r = 0.220, P = 0.002) and triglycerides (TGs, r = 0.295, P < 0.001), and TGs were an independent influencing factor of serum PNT levels in acromegalic subjects (P < 0.001). Furthermore, serum PNT levels in obese acromegalic patients were significantly higher than those with normal BMI (P < 0.05). However, serum furin levels were lower in acromegalic patients than controls (0.184 ± 0.036 vs. 0.204 ± 0.061 ng/ml, P < 0.001). CONCLUSION: This study is the first to demonstrate that acromegalic patients have increased serum PNT levels. Moreover, serum PNT plays a potential role in abnormal lipid metabolism of acromegalic patients.

Benefits of different combinations of aerobic and resistance exercise for improving plasma glucose and lipid metabolism and sleep quality among elderly patients with metabolic syndrome: a randomized controlled trial.

Exercise has beneficial effects on metabolic syndrome (MS). However, the exercise prescriptions that best support plasma glucose and lipid control remain unknown. We evaluated the effects of different combinations of aerobic and resistance training programs on plasma glucose and lipid metabolism and sleep quality in elderly MS patients. Eighty-five elderly MS patients were randomly assigned to five groups: aerobic training (AT), resistance training (RT), high aerobic with low resistance training (HALRT), high resistance with low aerobic training (HRLAT), or control. The exercise groups performed supervised moderate-intensity exercise during three 50-min sessions per week for 12 weeks. Body mass index (BMI), waist circumference (WC), systolic blood pressure (SBP), diastolic blood pressure (DBP), handgrip strength (HGS), fasting plasma glucose (FPG), 2-hour postprandial blood glucose (2hPG), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) levels and sleep quality were evaluated at baseline and after 12 weeks. All intervention groups showed significant improvements in SBP, HGS, FPG, 2hPG, and Pittsburgh Sleep Quality Index (PSQI) scores compared to baseline (all p < 0.05), while DBP, TC, TG, and LDL-C levels were significantly improved only in the HRLAT and HALRT groups (p < 0.05). The HALRT group showed the largest improvements in WC, SBP, DBP, HGS, FPG, 2hPG, and PSQI score (p < 0.001). The largest improvements in BMI, TC, and LDL-C were observed in the HRLAT group (p < 0.001). The combined exercise prescriptions were more effective than aerobic or resistance training alone at improving plasma glucose and lipid metabolism and sleep quality in elderly MS patients.

Peripheral Gonadotropin-Inhibitory Hormone (GnIH) Acting as a Novel Modulator Involved in Hyperphagia-Induced Obesity and Associated Disorders of Metabolism in an In Vivo Female Piglet Model.

Apart from the well-established role of the gonadotropin-inhibitory hormone (GnIH) in the regulation of the reproductive functions, much less is known about the peripheral role of the GnIH and its receptor in the metabolic processes. On account of pig being an excellent model for studies of food intake and obesity in humans, we investigated the peripheral effects of the GnIH on food intake and energy homeostasis and revealed the underlying mechanism(s) in female piglets in vivo. Compared to the vehicle-treated group, intraperitoneally injected GnIH significantly increased the food intake and altered the meal microstructure both in the fasting and ad libitum female piglet. GnIH-triggered hyperphagia induced female piglet obesity and altered islet hormone secretion in the pancreas, accompanied with dyslipidemia and hyperglycemia. Interestingly, GnIH decreased the glucose transport capacity and glycogen synthesis, whereas it increased the gluconeogenesis in the liver, while it also induced an insulin resistance in white adipose tissue (WAT) via inhibiting the activity of AKT-GSK3-ß signaling. In terms of the lipid metabolism, GnIH reduced the oxidation of fatty acids, whereas the elevated fat synthesis ability in the liver and WAT was developed though the inhibited AMPK phosphorylation. Our findings demonstrate that peripheral GnIH could trigger hyperphagia-induced obesity and an associated glycolipid metabolism disorder in female piglets, suggesting that GnIH may act as a potential therapeutic agent for metabolic syndrome, obesity and diabetes.

Marein ameliorates Ang II/hypoxia-induced abnormal glucolipid metabolism by modulating the HIF-1α/PPARα/γ pathway in H9c2 cells.

The objectives of this study were to investigate the effects of marein, a major bioactive compound in functional food Coreopsis tinctoria, in hypertrophic H9c2 cells. Treating angiotensin II/hypoxia-stimulated H9c2 cells with marein led to decreasing cell surface area, intracellular total protein, atrial natriuretic peptide, and free fatty acids levels, but increasing glucose level. Marein treatment decreased hypoxia inducible factor-1α (HIF-1α), peroxisome proliferator activated receptor γ (PPARγ), medium chain acyl-coenzyme A dehydrogenase, glucose transporter-4, and glycerol-3-phosphate acyltransferase protein expressions, and increased PPARα, fatty acid transport protein-1, carnitine palmitoyltransferase-1, and pyruvate dehydrogenase kinase-4 protein expressions. Similar results were observed in HIF-1α-overexpressing H9c2 cells, whereas these effects were abolished in siRNA-HIF-1α-transfected H9c2 cells. It was concluded that marein could ameliorate abnormal glucolipid metabolism in hypertrophic H9c2 cells, and the effects could be attributable to reduction of HIF-1α expression and subsequent regulation PPARα/γ-mediated lipogenic gene expressions.

[Correlation between thyroid function and glucolipid metabolism in type 1 diabetic adults].

To assess the correlation between thyroid function and glucolipid metabolism in type 1 diabetic adults. A retrospective analysis was conducted in 230 type 1 diabetic adults who were hospitalized in the Department of Endocrinology of Shandong Provincial Hospital Affiliated to Shandong University from January 2008 to January 2020. It showed that thyroid stimulating hormone(TSH) was significantly positively correlated with total cholesterol (TC) (r=0.239), triglycerides (TG) (r=0.166) and low-density lipoprotein cholesterol (LDL-C) (r=0.249), respectively (all P<0.05). Free triiodothyronine (FT3) was significantly negatively correlated with fasting plasma glucose (FPG) (r=-0.272), glycated hemoglobin (HbA1c) (r=-0.240), TC (r=-0.197) and LDL-C (r=-0.220), respectively (all P<0.05). Free thyroxine (FT4) was negatively correlated with TC (r=-0.171) and LDL-C (r=-0.170), respectively (all P<0.05). TC was an independent predictor of TSH, FT3 and FT4, FT3 and FT4 were independent predictors of HbA1c. TSH was an independent predictor of TC, TG and LDL-C. Thyroid function is closely related to glucolipid metabolism in type 1 diabetic adults.

[Effects of oral administration of ceftriaxone in early life on glucolipid metabolism of high fat diet-induced mice].

OBJECTIVE: This study aimed to explore whether exposure to ceftriaxone during early life could influences glucose and lipid metabolism of high fat diet-induced mice. METHODS: Total 48 of female BALB/c aged 2 week old were randomly divided into control group(treated with saline), antibiotic group(treated with100 mg/kg ceftriaxone), high-fat diet group(treated with saline) and combined action group(treated with 100 mg/kg ceftriaxone)(n=12), respectively to stop gavage 2 weeks later. Then high-fat diet group and combined action group were fed with high-fat diet for 12 weeks. Fasting blood glucose(FBG) and oral glucose tolerance test were conducted in the last week. Serum total cholesterol(TC), triglyceride(TG), high-density lipoprotein cholesterol(HDL-C), low-density lipoprotein cholesterol(LDL-C), fasting insulin, leptin and TG, TC in liver were also measured. Furthermore, homeostasis model assessment of insulin resistance(HOMA-IR) was calculated from FBG and insulin. RESULTS: Compared with normal chow diet, high-fat diet impaired oral glucose tolerance and increased the levels of abdominal adipose tissue, FBG, HOMA-IR, lips in serum and liver and leptin(P<0. 05). The oral administration of ceftriaxone in early life impaired oral glucose tolerance and increased the levels of abdominal adipose tissue, FBG and TG in liver(P<0. 05). In addition, early ceftriaxone intervention could enhance the impaired glucose tolerance, the increasing FBG, insulin resistance and liver lipids associated with high-fat diet(P<0. 05). CONCLUSION: Early ceftriaxone intervention not only significantly increases the level of abdominal adipose tissue, FBG, insulin resistance and liver lipids, but also enhances glycolipid metabolic disorders induced by high-fat diet. These result suggest that the exposure to antibiotics in the early life might increase the sensitivity of host animal to high fat diet induced abnormal glycolipid metabolism late.

[Effects of ω-3 polyunsaturated fatty acids from different sources on glucolipid metabolism in type 2 diabetic patients with dyslipidemia].

Objective: To determine the effects of ω-3 polyunsaturated fatty acids from different sources on glucolipid metabolism in type 2 diabetic patients with dyslipidemia. Methods: We recruited participants from the diabetes specialist clinic at the Guanlin hospital in Yixing city, Jiangsu Province from February 2017 to March 2017. A total of 180 subjects were randomly assigned to 3 g/day fish oil (FO), perilla oil (PO), or fish oil mixed with linseed oil (FLO) for 6 months. The basic conditions and fasting venous blood sample were obtained from each study subject at baseline, after 6 months of intervention. Serum glucose and lipid metabolism were investigated. Results: A total of 156 subjects aged (62.6±8.6) years completed the final follow-up after 6 months (FO,54 subjects; PO,52 subjects; FLO,50 subjects). Among them,59 patients (37.8%) were male. Serum glucose, glycated hemoglobin, C peptide, insulin and homeostasis model assessment-insulin resistance were not significantly different among the three groups after 6 months. Serum triglyceride decreased, whereas high-density lipoprotein cholesterol increased in FO [1.33 (1.05,1.93) mmol/L, (1.36±0.29) mmol/L, respectively] compared with PO [1.71 (1.23, 2.17) mmol/L, (1.23±0.22) mmol/L, respectively] and FLO [1.51 (1.12, 2.22) mmol/L, (1.29±0.30) mmol/L, respectively] (P<0.05). Serum low-density lipoprotein cholesterol and apolipoprotein B decreased in PO [(2.60±0.57) mmol/L,(0.96±0.23) g/L, respectively] compared with FO [(2.89±0.76) mmol/L, (1.07±0.30) g/L, respectively] (P<0.05). Serum lipoprotein(a) decreased in FLO [130.7 (63.3,270.6) mg/L] compared with FO [137.4 (58.7,333.2) mg/L] (P<0.05). Serum free fatty acid decreased in FLO [(0.43±0.15) mmol/L] compared with PO [(0.53±0.22) mmol/L] (P<0.05). Conclusion: The effects of ω-3 PUFA from different sources on glucose metabolism in type 2 diabetic patients with dyslipidemia are similar. Each of them has a good application prospect in improving lipid metabolism.

Chitosan Oligosaccharides Improve Glucolipid Metabolism Disorder in Liver by Suppression of Obesity-Related Inflammation and Restoration of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ).

Chitosan oligosaccharides (COS) display various biological activities. In this study, we aimed to explore the preventive effects of COS on glucolipid metabolism disorder using palmitic acid (PA)-induced HepG2 cells and high-fat diet (HFD)-fed C57BL/6J mice as experimental models in vitro and in vivo, respectively. The results showed that COS pretreatment for 12 h significantly ameliorated lipid accumulation in HepG2 cells exposed to PA for 24 h, accompanied by a reversing of the upregulated mRNA expression of proinflammatory cytokines (IL-6, MCP-1, TNF-α) and glucolipid metabolism-related regulators (SCD-1, ACC1, PCK1-α). In addition, COS treatment alleviated glucolipid metabolism disorder in mice fed with HFD for five months, including reduction in body weight and fasting glucose, restoration of intraperitoneal glucose tolerance, and suppression of overexpression of proinflammatory cytokines and glucolipid metabolism-related regulators. Furthermore, our study found that COS pretreatment significantly reversed the downregulation of PPARγ at transcriptional and translational levels in both PA-induced HepG2 cells and liver tissues of HFD-fed mice. In summary, the study suggests that COS can improve glucolipid metabolism disorder by suppressing inflammation and upregulating PPARγ expression. This indicates a novel application of COS in preventing and treating glucolipid metabolism-related diseases.