scholarly journals Peran Mikrobiota Usus Terhadap kondisi Obesitas

2020 ◽  
pp. 31-42
Author(s):  
Armanto Makmun ◽  
Wialda Dwi Rodya ◽  
Zulfahmidah Zulfahmidah ◽  
Windy Nurul Aisyah Aisyah
Keyword(s):  
Insulin Resistance ◽  
Food Intake ◽  
Gut Microbiota ◽  
Signaling Molecules ◽  
Low Grade ◽  
Energy Regulation ◽  
Paracrine Signaling ◽  
Obese People ◽  
Peptide Signaling ◽  
Bacterial Products

The gut microbiota has been recognized as an important factor in the development of metabolic diseases such as obesity and is considered an endocrine organ involved in the maintenance of energy homeostasis and immunity. Intestinal dysbiosis can alter gastrointestinal peptide production associated with satiety, resulting in increased food intake. In obese people, this dysbiosis appears to be associated with increased gut microbiota has been implicated in the control of food intake and satiety via intestinal peptide signaling, in which bacterial products activate enteroen-docrine cells by modulating enterocyte-produced paracrine signaling molecules. The gut microbiota can increase the production of certain SCFAs, which have been shown to be associated with increased production of YY (PYY) peptides, ghrelin, insulin, and glucagon-like peptide-1 (GLP-1). The purpose of this study was to Article Review by looking at the topic of the gut microbiota and obesity by using research with quantitative meta-analysis methods based on previous research. This research method uses the article review method. The data source of this research comes from literature obtained via the internet in the form of research results from international journals in 2010-2020. The results of this study from a total of 50 journals, which the authors have reviewed, concluded that the role of the gut microbiota in energy regulation, studies have linked the gut microbiota with the pathogenesis of insulin resistance and inflammation in obesity. It is known that obesity is associated with low-grade chronic inflammation and insulin resistance. The gut microbiota has been implicated in the control of food intake and satiety through intestinal peptide signaling, in which bacterial products activate enteroen-docrine cells by modulating the enterocyte-produced paracrine signaling molecules. The conclusion of this study based on the results of the study found that the effect of intestinal microbiotas on obesity.

Effects of flavonoids on intestinal inflammation, barrier integrity and changes in gut microbiota during diet-induced obesity

2016 ◽  
Vol 29 (2) ◽  
pp. 234-248 ◽  
Author(s):  
Katherine Gil-Cardoso ◽  
Iris Ginés ◽  
Montserrat Pinent ◽  
Anna Ardévol ◽  
Mayte Blay ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Intestinal Inflammation ◽  
Mucosal Barrier ◽  
Low Grade ◽  
Protective Effects ◽  
Barrier Integrity ◽  
Diet Induced Obesity

AbstractDiet-induced obesity is associated with low-grade inflammation, which, in most cases, leads to the development of metabolic disorders, primarily insulin resistance and type 2 diabetes. Although prior studies have implicated the adipose tissue as being primarily responsible for obesity-associated inflammation, the latest discoveries have correlated impairments in intestinal immune homeostasis and the mucosal barrier with increased activation of the inflammatory pathways and the development of insulin resistance. Therefore, it is essential to define the mechanisms underlying the obesity-associated gut alterations to develop therapies to prevent and treat obesity and its associated diseases. Flavonoids appear to be promising candidates among the natural preventive treatments that have been identified to date. They have been shown to protect against several diseases, including CVD and various cancers. Furthermore, they have clear anti-inflammatory properties, which have primarily been evaluated in non-intestinal models. At present, a growing body of evidence suggests that flavonoids could exert a protective role against obesity-associated pathologies by modulating inflammatory-related cellular events in the intestine and/or the composition of the microbiota populations. The present paper will review the literature to date that has described the protective effects of flavonoids on intestinal inflammation, barrier integrity and gut microbiota in studies conducted using in vivo and in vitro models.

Adipose Tissue Hormones and Appetite and Body Weight Regulators an Insulin Resistance / Гормоны Жировой Ткани И Регуляторы Аппетита И Массы Тела При Инсулиновой Резистентности

Folia Medica ◽  
2013 ◽  
Vol 55 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Daniela Iv. Koleva ◽  
Maria M. Orbetzova ◽  
Pepa K. Atanassova
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Body Mass ◽  
Polycystic Ovary ◽  
Dependent Diabetes Mellitus ◽  
Obese People ◽  
Obesity And Diabetes ◽  
Tissue Hormones

Abstract Impaired sensitivity to insulin (the so called insulin resistance, IR) occurs in a number of genetic and acquired conditions, including obesity, non-insulin dependent diabetes mellitus, polycystic ovary syndrome (PCOS) and metabolic syndrome (MS). In this review we discuss the correlation between IR, the adipose tissue hormones and appetite and body weight regulators. Leptin acts as a major adipostat: it suppresses food intake and activates catabolic pathways associated with increased energy production. It improves the peripheral insulin sensitivity and affects β-cell function. Adiponectin is the only adipocytokine discovered so far that has anti-atherogenic properties. There is a reverse correlation between the serum adiponectin levels and the degree of obesity, IR, impaired glucose tolerance, dyslipidemia and atherosclerosis. Ghrelin stimulates food intake; of all circulating orexigenic hormones ghrelin is the most thoroughly studied. Ghrelin levels are decreased in MS and PCOS patients as this hormone is negatively correlated with body mass. Resistin is a hormone secreted by adipose tissues; a growing body of evidence suggests that it might be implicated in the link between obesity and diabetes. It has been found that the hormone‘s levels are significantly higher in obese people than those in normal body mass people. The recently discovered adipose tissue hormones, vaspin, visfatin, omentin-1 and their effect on IR development, have been increasingly researched.

scholarly journals Role of Dietary Lipids in Modulating Inflammation through the Gut Microbiota

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 117 ◽  
Author(s):  
Paul J. Wisniewski ◽  
Robert A. Dowden ◽  
Sara C. Campbell
Keyword(s):  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Current Knowledge ◽  
Endocannabinoid System ◽  
Dietary Lipids ◽  
Taxonomic Resolution ◽  
Low Grade ◽  
Energy Regulation ◽  
Microbial Dysbiosis

Inflammation and its resolution is a tenuous balance that is under constant contest. Though several regulatory mechanisms are employed to maintain homeostasis, disruptions in the regulation of inflammation can lead to detrimental effects for the host. Of note, the gut and microbial dysbiosis are implicated in the pathology of systemic chronic low-grade inflammation which has been linked to several metabolic diseases. What remains to be described is the extent to which dietary fat and concomitant changes in the gut microbiota contribute to, or arise from, the onset of metabolic disorders. The present review will highlight the role of microorganisms in host energy regulation and several mechanisms that contribute to inflammatory pathways. This review will also discuss the immunomodulatory effects of the endocannabinoid system and its link with the gut microbiota. Finally, a brief discussion arguing for improved taxonomic resolution (at the species and strain level) is needed to deepen our current knowledge of the microbiota and host inflammatory state.

scholarly journals TLR4 at the Crossroads of Nutrients, Gut Microbiota, and Metabolic Inflammation

2015 ◽  
Vol 36 (3) ◽  
pp. 245-271 ◽  
Author(s):  
Licio A. Velloso ◽  
Franco Folli ◽  
Mario J. Saad
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Gut Microbiota ◽  
Intestinal Barrier ◽  
Current Data ◽  
Dietary Fats ◽  
Low Grade ◽  
Metabolic Inflammation

Abstract Obesity is accompanied by the activation of low-grade inflammatory activity in metabolically relevant tissues. Studies have shown that obesity-associated insulin resistance results from the inflammatory targeting and inhibition of key proteins of the insulin-signaling pathway. At least three apparently distinct mechanisms–endoplasmic reticulum stress, toll-like receptor (TLR) 4 activation, and changes in gut microbiota–have been identified as triggers of obesity-associated metabolic inflammation; thus, they are expected to represent potential targets for the treatment of obesity and its comorbidities. Here, we review the data that place TLR4 in the center of the events that connect the consumption of dietary fats with metabolic inflammation and insulin resistance. Changes in the gut microbiota can lead to reduced integrity of the intestinal barrier, leading to increased leakage of lipopolysaccharides and fatty acids, which can act upon TLR4 to activate systemic inflammation. Fatty acids can also trigger endoplasmic reticulum stress, which can be further stimulated by cross talk with active TLR4. Thus, the current data support a connection among the three main triggers of metabolic inflammation, and TLR4 emerges as a link among all of these mechanisms.

scholarly journals Therapeutic Effect of Cucumis melo L. Extract on Insulin Resistance and the Gut Microbiome in Lepob/Lepob Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Daeun Lee ◽  
Jung Hwa Yoo ◽  
Byung-Cheol Lee
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
Cucumis Melo ◽  
Causative Factor ◽  
Microbiota Composition ◽  
Obese People ◽  
Inflammatory State ◽  
Composition Ratios

Obesity results in the progression of metabolic disorders, especially type 2 diabetes (T2DM). Obesity-induced insulin resistance (IR) is a causative factor of T2DM morbidity in obese people. It is generally held by clinicians that IR is caused by adiposity-related inflammation that is mediated by changes in composite ions in the gut microbiome. This experimental study was designed to investigate the effects of Cucumis melo L. (Cucumis) on obesity-induced IR in genetically leptin-deficient Lepob/Lepob mice. Specifically, we examined the anti-inflammatory effects of Cucumis and the effects of Cucumis on the gut microbiota. We evaluated glucose control by measuring FBS, performing the OGTT, quantifying serum IR, calculating the HOMA-IR, and determining the lipid profiles. To see whether inflammation was reduced, we analyzed adipose tissue macrophages as well as monocytes in the blood. We also profiled the gut microbiota to determine whether the ratios of microbial phyla changed. We found that Cucumis improved IR in obese mice and relieved inflammation in adipose tissue and blood. Simultaneously, the microbiota composition ratios changed. In conclusion, administration of Cucumis improved IR by reducing inflammation, thereby changing the gut microbiota composition. Cucumis is thus a promising treatment for obesity-induced insulin resistance and the inflammatory state.

scholarly journals Mechanistically different effects of fat and sugar on insulin resistance, hypertension, and gut microbiota in rats

2018 ◽  
Vol 314 (6) ◽  
pp. E552-E563 ◽  
Author(s):  
Sara Ramos-Romero ◽  
Mercè Hereu ◽  
Lidia Atienza ◽  
Josefina Casas ◽  
Olga Jáuregui ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Systemic Inflammation ◽  
Dietary Fat ◽  
Short Chain Fatty Acids ◽  
Low Grade ◽  
Long Term Effects ◽  
Inflammatory Infiltration ◽  
Wky Rats ◽  
Wistar Kyoto

Insulin resistance (IR) and impaired glucose tolerance (IGT) are the first manifestations of diet-induced metabolic alterations leading to Type 2 diabetes, while hypertension is the deadliest risk factor of cardiovascular disease. The roles of dietary fat and fructose in the development of IR, IGT, and hypertension are controversial. We tested the long-term effects of an excess of fat or sucrose (fructose/glucose) on healthy male Wistar-Kyoto (WKY) rats. Fat affects IR and IGT earlier than fructose through low-grade systemic inflammation evidenced by liver inflammatory infiltration, increased levels of plasma IL-6, PGE2, and reduced levels of protective short-chain fatty acids without triggering hypertension. Increased populations of gut Enterobacteriales and Escherichia coli may contribute to systemic inflammation through the generation of lipopolysaccharides. Unlike fat, fructose induces increased levels of diacylglycerols (lipid mediators of IR) in the liver, urine F2-isoprostanes (markers of systemic oxidative stress), and uric acid, and triggers hypertension. Elevated populations of Enterobacteriales and E. coli were only detected in rats given an excess of fructose at the end of the study. Dietary fat and fructose trigger IR and IGT in clearly differentiated ways in WKY rats: early low-grade inflammation and late direct lipid toxicity, respectively; gut microbiota plays a role mainly in fat-induced IR, and hypertension is independent of inflammation-mediated IR. The results provide evidence that suggests that the combination of fat and sugar is potentially more harmful than fat or sugar alone when taken in excess.

scholarly journals State of the micro-biota of bowels with dislipidemii in the children

2019 ◽  
pp. 76-82
Author(s):  
L. A. Kharitonova ◽  
O. V. Papisheva ◽  
T. A. Mayatskaya ◽  
G. A. Kotaysh
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Chronic Disease ◽  
Gut Microbiota ◽  
Metabolic Disorders ◽  
Low Grade ◽  
Gut Permeability ◽  
Pathological Conditions ◽  
Low Grade Inflammation

The gut microbiota has attracted increasing attention during the last several years as a key player in the pathophysiology of chronic disease. Microbiome is considered to be the link between metabolic disorders, obesity, insulin resistance, dyslipidemia, diabetes, hypertension and cardiovascular diseases. Recent findings have related the intestinal microbiota to a plethora of pathological conditions, including type 2 diabetes, obesity, cholelithiasis and nonalcoholic steatohepatitis. This review presents potential mechanisms for the development of these diseases in response to changes in the gut microbiota. They involve increased gut permeability, low-grade inflammation and autoantibodies. Many studies contradict each other, which confirms the need for further scientific research in this area.

Folate and vitamin B-12 deficiencies additively impaired memory function and disturbed the gut microbiota in amyloid-β infused rats

2019 ◽  
pp. 1-13 ◽  
Author(s):  
Sunmin Park ◽  
Sunna Kang ◽  
Da Sol Kim
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Insulin Signaling ◽  
Gut Microbiome ◽  
Metabolic Diseases ◽  
Memory Function ◽  
Amyloid Β ◽  
Impaired Memory ◽  
Ca1 Region ◽  
Folate And Vitamin B12

Abstract. Folate and vitamin B12(V-B12) deficiencies are associated with metabolic diseases that may impair memory function. We hypothesized that folate and V-B12 may differently alter mild cognitive impairment, glucose metabolism, and inflammation by modulating the gut microbiome in rats with Alzheimer’s disease (AD)-like dementia. The hypothesis was examined in hippocampal amyloid-β infused rats, and its mechanism was explored. Rats that received an amyloid-β(25–35) infusion into the CA1 region of the hippocampus were fed either control(2.5 mg folate plus 25 μg V-B12/kg diet; AD-CON, n = 10), no folate(0 folate plus 25 μg V-B12/kg diet; AD-FA, n = 10), no V-B12(2.5 mg folate plus 0 μg V-B12/kg diet; AD-V-B12, n = 10), or no folate plus no V-B12(0 mg folate plus 0 μg V-B12/kg diet; AD-FAB12, n = 10) in high-fat diets for 8 weeks. AD-FA and AD-VB12 exacerbated bone mineral loss in the lumbar spine and femur whereas AD-FA lowered lean body mass in the hip compared to AD-CON(P < 0.05). Only AD-FAB12 exacerbated memory impairment by 1.3 and 1.4 folds, respectively, as measured by passive avoidance and water maze tests, compared to AD-CON(P < 0.01). Hippocampal insulin signaling and neuroinflammation were attenuated in AD-CON compared to Non-AD-CON. AD-FAB12 impaired the signaling (pAkt→pGSK-3β) and serum TNF-α and IL-1β levels the most among all groups. AD-CON decreased glucose tolerance by increasing insulin resistance compared to Non-AD-CON. AD-VB12 and AD-FAB12 increased insulin resistance by 1.2 and 1.3 folds, respectively, compared to the AD-CON. AD-CON and Non-AD-CON had a separate communities of gut microbiota. The relative counts of Bacteroidia were lower and those of Clostridia were higher in AD-CON than Non-AD-CON. AD-FA, but not V-B12, separated the gut microbiome community compared to AD-CON and AD-VB12(P = 0.009). In conclusion, folate and B-12 deficiencies impaired memory function by impairing hippocampal insulin signaling and gut microbiota in AD rats.

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