scholarly journals EVALUATION OF CYCLIC ADENOSINE MONOPHOSPHATE AND NEUROTRANSMITTERS IN EXPERIMENTAL OBESITY: IMPACT OF BLACK PEPPER AND COFFEE AQUEOUS EXTRACTS

2016 ◽  
Vol 9 (9) ◽  
pp. 87 ◽  
Author(s):  
Yasmin Abdel Latif ◽  
Shadia Fathy ◽  
Zakaria El-khayat ◽  
Maha Moustafa ◽  
Abdel Razik Farrag ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Lipid Profile ◽  
High Performance ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Black Pepper

ABSTRACTObjective: This study aims to evaluate the effect of black pepper and coffee extracts on chronic and acute experimental-induced obesity and energyhomeostasis.Methods: Rats were divided into 10 groups including control, high-fat diet (HFD), triton, HFD+triton, black pepper+HFD, black pepper+HFD+triton,coffee+HFD, coffee+HFD+triton, mixture+HFD, and mixture+HFD+triton groups. Blood glucose, serum insulin, and insulin resistance were estimated.Body mass index, food efficiency intake, and body weight gain were calculated. Lipid profile, liver and kidney functions were measured, serum and braincyclic adenosine monophosphate (cAMP) was estimated, and brain neurotransmitters were measured by high-performance liquid chromatography.Furthermore, histopathology of liver was performed.Results: Findings showed that blood glucose, insulin resistance, lipid profile, kidney and liver functions as well as brain cAMP and neurotransmitterswere significantly increased, concomitant with a significant decrease in insulin resistance and serum cAMP in both HFD and triton-induced obesitygroups compared to control.Conclusion: Supplementation with black pepper extract, coffee extract, and a mixture of both significantly improved these findings. In conclusion,black pepper and coffee extracts are overlooked as promising weight reduction and antihyperlipidemic agents.Keywords: Energy homeostasis, Obesity, Black pepper extract, Coffee extract, Cyclic adenosine monophosphate, Neurotransmitters.

scholarly journals Role of Long Non-Coding RNAs and the Molecular Mechanisms Involved in Insulin Resistance

2021 ◽  
Vol 22 (14) ◽  
pp. 7256
Author(s):  
Vianet Argelia Tello-Flores ◽  
Fredy Omar Beltrán-Anaya ◽  
Marco Antonio Ramírez-Vargas ◽  
Brenda Ely Esteban-Casales ◽  
Napoleón Navarro-Tito ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protein Kinase ◽  
Molecular Mechanisms ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Biological Species ◽  
Necrosis Factor Alpha ◽  
Polypyrimidine Tract Binding Protein ◽  
Non Coding Rnas

Long non-coding RNAs (lncRNAs) are single-stranded RNA biomolecules with a length of >200 nt, and they are currently considered to be master regulators of many pathological processes. Recent publications have shown that lncRNAs play important roles in the pathogenesis and progression of insulin resistance (IR) and glucose homeostasis by regulating inflammatory and lipogenic processes. lncRNAs regulate gene expression by binding to other non-coding RNAs, mRNAs, proteins, and DNA. In recent years, several mechanisms have been reported to explain the key roles of lncRNAs in the development of IR, including metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), imprinted maternal-ly expressed transcript (H19), maternally expressed gene 3 (MEG3), myocardial infarction-associated transcript (MIAT), and steroid receptor RNA activator (SRA), HOX transcript antisense RNA (HOTAIR), and downregulated Expression-Related Hexose/Glucose Transport Enhancer (DREH). LncRNAs participate in the regulation of lipid and carbohydrate metabolism, the inflammatory process, and oxidative stress through different pathways, such as cyclic adenosine monophosphate/protein kinase A (cAMP/PKA), phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT), polypyrimidine tract-binding protein 1/element-binding transcription factor 1c (PTBP1/SREBP-1c), AKT/nitric oxide synthase (eNOS), AKT/forkhead box O1 (FoxO1), and tumor necrosis factor-alpha (TNF-α)/c-Jun-N-terminal kinases (JNK). On the other hand, the mechanisms linked to the molecular, cellular, and biochemical actions of lncRNAs vary according to the tissue, biological species, and the severity of IR. Therefore, it is essential to elucidate the role of lncRNAs in the insulin signaling pathway and glucose and lipid metabolism. This review analyzes the function and molecular mechanisms of lncRNAs involved in the development of IR.

scholarly journals Hypoglycemic Effect of Vitexin in C57BL/6J Mice and HepG2 Models

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Weidong Xu ◽  
Jiayao Li ◽  
Weipeng Qi ◽  
Ye Peng
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Weight Gain ◽  
Blood Glucose ◽  
Glucose Uptake ◽  
Lipid Content ◽  
Hepg2 Cells ◽  
Body Weight Gain ◽  
Tnf Α ◽  
Hepatic Lipid Content

Apigenin-8-C-glucoside (vitexin), a natural phytochemical contained in hawthorn, has been reported to have versatile beneficial bioactivities, such as antioxidation, anticancer property, and adipogenesis inhibition. The present research aimed to determine the influence of vitexin on insulin resistance elicited by HFD in mice and HepG2 cells. Vitexin markedly alleviated body weight gain and improved glucose and insulin intolerance induced by HFD. Vitexin partially normalized blood glucose, cholesterol, TNF-α, and hepatic lipid content. Moreover, vitexin recovered the reduced glucose uptake induced by glucosamine. The present results indicate that vitexin prevents HFD-induced insulin resistance.

scholarly journals Adiponectin, an Adipocyte-Derived Protein, Predicts Future Insulin Resistance: Two-Year Follow-Up Study in Japanese Population

2004 ◽  
Vol 89 (1) ◽  
pp. 87-90 ◽  
Author(s):  
Yukihiro Yamamoto ◽  
Hiroshi Hirose ◽  
Ikuo Saito ◽  
Kanako Nishikai ◽  
Takao Saruta
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Lipid Profile ◽  
Adiponectin Level ◽  
Serum Insulin ◽  
Resistance Index ◽  
Serum Adiponectin ◽  
Model Assessment ◽  
Homeostasis Model Assessment ◽  
Insulin Resistance Index

It has been reported that the serum adiponectin level was negatively correlated with body mass index (BMI), insulin resistance index, and triglycerides and was positively correlated with high-density lipoprotein cholesterol in several cross-sectional studies. However, the causal relationship has not been elucidated. We investigated whether the baseline adiponectin level could predict subsequent changes in insulin resistance, lipid profile, or body weight in a 2-yr longitudinal study. This study included 590 male Japanese subjects, aged 30–65 yr, who received annual health checkups in both 2000 and 2002. Blood pressure, heart rate, and anthropometric and metabolic parameters, including serum insulin and adiponectin levels, were determined. The insulin resistance index was calculated based on homeostasis model assessment. Baseline adiponectin level was not correlated with the subsequent change in lipid profile or BMI in 2 yr after adjustment for each baseline value. However, the baseline adiponectin level was negatively correlated with subsequent changes in insulin and insulin resistance index based on homeostasis model assessment, even after adjustment for change in BMI (r = −0.162 and r = −0.140, respectively). These findings suggest that the serum adiponectin concentration predicts subsequent changes in insulin resistance, but not in lipid profile or body weight.

scholarly journals A new way for punicalagin to alleviate insulin resistance: regulating gut microbiota and autophagy

2021 ◽  
Author(s):  
Yuan Cao ◽  
Guofeng Ren ◽  
Yahui Zhang ◽  
Hong Qin ◽  
Xin An ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Injury ◽  
Gut Microbiota ◽  
Research Study ◽  
Inflammatory Responses ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Pomegranate Juice ◽  
Rrna Gene ◽  
Lipid Metabolism Disorder

Background: Insulin resistance, defined as a diminished ability to respond to the stimulation of insulin, is the main line for a variety of metabolic-related diseases. Punicalagin (PU), a hydrolyzable tannin of pomegranate juice, exhibits multiple biological properties, including anti-oxidant, anti-cancer and anti-inflammatory activities. Objective: This research study aimed at determining the protective effect of PU on insulin resistance and to uncover the underlying mechanism based on the gut microbiota, IKKβ/NF-κB pathway, and autophagy. Design: An insulin resistance animal model was established using C57BL/6 mice fed with a high-fat diet (HFD) for 8 weeks. The model included two groups continuing a HFD for 12 weeks with or without administering via gavage with PU 20 mg/kg/day. Changes in fasting plasma glucose levels, fasting serum insulin levels, glucose and insulin tolerance, glycolipid metabolism, gut microbiota composition (16S rRNA gene sequencing), inflammatory responses, and autophagy in the liver were evaluated. Body weight gain, glycolipid metabolic disorder, liver injury, as well as systemic and hepatic insulin sensitivity, were significantly attenuated after supplementing with PU. Results: This research study revealed that PU alleviated HFD-induced glucose and lipid disorders, liver injury and insulin resistance; decreased the Firmicutes/Bacteroides ratio, decreased the abundance of Coprococcus and Anaerotruncus, and increased Rikenellaceae; and decreased serum and liver tumor necrosis factor-alpha and interleukin-1β levels, inhibited liver IKKβ and NF-κB phosphorylation; and increased liver autophagy-related proteins LC3-II, P62, and Beclin1, and increased the number of liver autophagosomes. Conclusion: PU can improve HFD-induced insulin resistance, improved liver glucose and lipid metabolism disorder and liver injury, and the potential mechanism is that PU inhibited the IKKβ/NF-κB inflammatory pathway by regulating gut microbiota homeostasis and up-regulating liver autophagy

scholarly journals Mu opioid receptors acutely regulate adenosine signaling in a thalamo-striatal circuit.

2021 ◽  
Author(s):  
Sweta Adhikary ◽  
William T Birdsong
Keyword(s):  
Opioid Receptors ◽  
Neurotransmitter Release ◽  
Energy Homeostasis ◽  
Prolonged Exposure ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Mu Opioid Receptors ◽  
Presynaptic Terminals ◽  
Mu Opioid ◽  
Adenosine Signaling

Endogenous adenosine plays a crucial role in maintaining energy homeostasis and adenosine levels are tightly regulated across neural circuits. In the dorsal medial striatum (DMS) adenosine inhibits neurotransmitter release, but the source and mechanism underlying its accumulation are largely unknown. Opioids also inhibit neurotransmitter release in the DMS and influences adenosine accumulation after prolonged exposure. However, how these two neurotransmitter systems interact acutely is also largely unknown. This study demonstrates that activation of mu opioid receptors (MORs), but not delta opioid receptors (DORs) or kappa opioid receptors (KORs), inhibits tonic activation of adenosine A1Rs via a cyclic adenosine monophosphate (cAMP) dependent mechanism in both male and female mice. Further, selectively knocking-out MORs from presynaptic terminals and postsynaptic medium spiny neurons (MSNs) revealed that activation of MORs on D1R positive MSNs, but not D2R positive MSNs, is necessary to inhibit tonic adenosine signaling on presynaptic terminals. Given the role of D1R positive MSNs in movement and motivated behaviors, these findings reveal a novel mechanism by which these neurons regulate their own synaptic inputs.

scholarly journals Effects of Omega-3 Fatty Acids on Insulin Resistance in an Ovariectomized Mouse Model of Diet-Induced Obesity Treated with Chemotherapy

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 345-345
Author(s):  
Kate Ormiston ◽  
Zihan Zhang ◽  
Kelly Murphy ◽  
A Courtney DeVries ◽  
Maryam Lustberg ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Blood Glucose ◽  
Body Fat ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Model Assessment ◽  
Omega 3 ◽  
High Fat ◽  
Body Weights

Abstract Objectives Our objective was to examine effects of dietary enrichment of eicosapentaenoic acid + docosahexaenoic acid (EPA + DHA) on high fat diet-induced insulin resistance during chemotherapy. Methods Adult, female C57Bl/6 mice (n = 48) were assigned to 1 of 3 diets; low-fat diet (LF; 10% kcals fat), high-fat diet (HF; 45% kcals fat), or HF diet with omega-3 s (HF n-3; 2% kcals EPA + DHA) for 7 weeks. Mice received vehicle or chemotherapy injections (doxorubicin + cyclophosphamide), by tail vein at week 4 and 6. Food intake and body weights were recorded. Fasted blood glucose and serum insulin were measured weekly.  Homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. Body composition was measured using Echo MRI. Data were analyzed using ANOVA; p < 0.05 was considered significant. Results Total kilocalories significantly differed by group (p < 0.001); HF and HF n-3 groups consumed more than the LF group (p < 0.001, p < 0.0001; respectively). Obesity was induced prior to first injection with body weights being significantly different (p < 0.01); the LF group weighed less than the HF n-3 group (p < 0.01), and there was a similar trend between LF and HF groups (p = 0.0519). Body weights at sacrifice significantly differed (p < 0.0001); chemotherapy mice weighed less than vehicle (p < 0.0001). Percent body fat at sacrifice significantly differed (p < 0.0001); chemotherapy mice had less fat than vehicle (p < 0.0001), and the LF group had less fat than HF  (p < 0.01) and HF n-3 group (p < 0.01). Blood glucose significantly differed at sacrifice (p < 0.01); chemotherapy mice had lower glucose than vehicle (p < 0.05) and HF group had higher glucose than LF group (p < 0.01). HOMA-IR scores at sacrifice significantly differed (p < 0.05); chemotherapy mice had lower scores than vehicle  (p < 0.05) and mice on the LF and HF n-3 diets had lower scores than the HF diet (p < 0.01; p < 0.05 respectively). Conclusions Chemotherapy lowered body weight and body fat in mice, potentially contributing to decreases in blood glucose and insulin resistance. EPA + DHA enrichment of a HF diet reduced insulin resistance in mice comparable to a LF diet group. This occurred in both chemotherapy and vehicle treated mice, despite LF diet-fed mice having lower body weight and adiposity. Underlying mechanisms are being investigated. Funding Sources NIH #5R01CA18994.

scholarly journals Short-term high-fat feeding induces islet macrophage infiltration and β-cell replication independently of insulin resistance in mice

2016 ◽  
Vol 311 (4) ◽  
pp. E763-E771 ◽  
Author(s):  
David C. Woodland ◽  
Wei Liu ◽  
Jacky Leong ◽  
Mallory L. Sears ◽  
Ping Luo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Serum Insulin ◽  
Cell Replication ◽  
Fat Pad ◽  
High Fat ◽  
Fasting Serum ◽  
Β Cell ◽  
Short Term ◽  
Insulin Levels

Short-term high-fat consumption stimulates mouse islet β-cell replication through unknown mechanisms. Resident macrophages (MΦs) are capable of secreting various factors involved in islet development and tissue remodeling. We hypothesized that a short-term high-fat diet (HFD) promotes MΦ infiltration in pancreatic islets and that MΦs serve as a regulator of β-cell replication. To test these hypotheses and dissect mechanisms involved in HFD-induced β-cell replication, adult C57BL/6J mice were fed a HFD for 7 days with or without administration of clodronate-containing liposomes, an MΦ-depleting agent. Mouse body and epididymal fat pad weights, and nonfasting blood glucose and fasting serum insulin levels were measured, and pancreatic islet β-cell replication, oxidative stress, and MΦ infiltration were examined. Short-term HFD promoted an increase in body and epididymal fat pad weight and blood glucose levels, along with an increased fasting serum insulin concentration. β-Cell replication, islet MΦ infiltration, and the percentage of inducible NO synthase positive MΦs in the islets increased significantly in mice fed the HFD. Immunofluorescence staining for 8-oxo-2′-deoxyguanosine or activated caspase-3 revealed no significant induction of DNA damage or apoptosis, respectively. In addition, no change in stromal-derived factor 1-expressing cells was found induced by HFD. Despite continuous elevation of nonfasting blood glucose and fasting serum insulin levels, depletion of MΦs through treatments of clodronate abrogated HFD-induced β-cell replication. These findings demonstrated that HFD-induced MΦ infiltration is responsible for β-cell replication. This study suggests the existence of MΦ-mediated mechanisms in β-cell replication that are independent of insulin resistance.

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