Obesity And Gut Microbiota Pdf


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obesity and gut microbiota pdf

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Between 1, and 1, bacterial species have potential to colonise the human gastro-intestinal GI tract, with each individual harbouring around different species 1. The composition of the gut microbiota has received attention as an etiological factor in the development of obesity.

Malnutrition through excessive food consumption is a worldwide pandemic.

Obesity is abnormal or excessive fat accumulation that is associated with progression of metabolic diseases including type 2 diabetes mellitus, cardiovascular disease, nonalcoholic fatty liver disease, and cancer. Gut microbiota GM have received much attention as essential factors in development and progression of obesity. The diversity, composition, and metabolic activity of GM are closely associated with nutrient intake and dietary pattern. Scientific evidence supports the idea that dietary pattern directly changes the GM profile; therefore, diet is a crucial component related to interactions between GM and obesity progression.

Gut microbiota: a new path to treat obesity

Probiotics are now recognized for several health benefits and they have been recommended as a complementary therapeutic agent for metabolic disorders. Obesity is an altered health condition, which is a resultant of irregular energy intake and energy balance, changes in gut microbiota, and improper diet with the influence of genetic makeup and environmental factors.

Several studies revealed the influence of probiotic supplementation on obesity-associated consequences in vitro , in vivo , and in human clinical studies. The current manuscript discussed the factors influencing the occurrence of obesity, the interplay between microbiome and obesity, the effect of the probiotic intervention on the health status of obese people, and possible mechanism of antiobesity activity of probiotics.

The literature survey revealed that the antiobese activity of probiotics might be associated with their ability to alter the intestinal microbiota, remodeling of energy metabolism, alter the expression of genes related to thermogenesis, glucose metabolism, and lipid metabolism, and change the parasympathetic nerve activity.

Further intense research is necessary to figure out the best probiotic or synbiotic mixture and optimum dosage and duration of the intervention to reduce obesity and prevent the recurring of obese condition.

Food habits and lifestyle greatly influence the quality of the life and health status of humans. The improper diet and lifestyle are associated with several metabolic disorders and are the greatest global health issues [ 1 ].

The environmental factors, maternal health, and host genetic makeup are also involved in the development of metabolic disorders and diseases. The composition of gut microbiota GM and its function is altered due to the consumption of improper diet, which affects the health status of the host, specifically associated with the development of obesity. GM is involved in the energy balancing, intestinal integrity, and immunity against invading pathogens; thereby GM controls the overall health status of the host [ 2 — 4 ].

GM can be positively altered by the supplementation of probiotics, a group of beneficial microbes that confers health benefits when consumed in an adequate amount [ 5 ].

Probiotic intervention has been recognized for the treatment or betterment of several ill-health conditions such as diarrhea, allergy, gastrointestinal disorders, and metabolic syndromes [ 6 — 11 ]. The probiotic supplementation also slows down the aging-associated health issues by positive regulation of GM [ 12 , 13 ].

Obesity is an altered health condition, which is a resultant of irregular energy intake and energy balance, changes in GM, and improper diet with the influence of genetic makeup and environmental factors.

Obesity is defined as an accumulation of excessive fat that impairs health status [ 14 ]. The obesity rate is drastically increased over the last decades [ 15 ], and it has been estimated that about 1. The overweight with some ill-health conditions such as diabetes, hypertension, and cardiovascular diseases is considered as morbid obesity [ 14 , 17 ].

GM is one of the influencing environmental factors involved in the initiation of obesity mainly by disturbing the food intake and energy balance. Though some of the in vivo studies demonstrated the role of GM in the onset of obesity, the exact etiology of obesity has not yet been explained [ 2 , 14 , 18 , 19 ]. As mentioned earlier, probiotic is a feasible way to regulate and improve the GM. In recent decades, several studies have focused on the influence of probiotic supplementation on the health improvement of obese people, and the results were found to be controversial.

The current manuscript summarizes and discusses the outcome of clinical trials conducted to evaluate the probiotic based supplementation on the health status of obese people. Several factors are associated with the development of obesity. Use of high-calorie fast-foods, high consumption rate, less physical powered occupations, lack of physical activities, insufficient sleep, side effects from the medicines like topiramate, olanzapine, and pioglitazone, and other environmental, genetic, and socioeconomic factors are closely related to the onset of obesity [ 20 — 23 ].

Energy imbalance, environmental factors, and genetic makeup are significantly connected to a network that regulates several physiological functions. The neuronal system regulates the energy expenditure through the stimulants from the gastrointestinal tract in the form of neurotransmitters and other neuropeptides produced by GM.

The regulatory molecules released by the microbiota influence the brain regions, which is responsible for cognitive functions, emotions, and food consumption. The negative energy balance due to increased physical activity or reduced food consumption or both plays a vital role in obesity in association with energy expenditure, physical and metabolic activities, and orexigenic signals [ 55 — 59 ].

Pigeyre et al. The mutation in leptin leptin is an adipocyte-specific secreted protein associated with energy expenditure and appetite , leptin receptor, melanocortin 4 receptor a G-protein-coupled receptor implicated in energy homeostasis , and prohormone convertase 1 involved in managing prohormones , defects in proopiomelanocortin precursor precursor of adrenocorticotrophin, melanocyte-stimulating hormones, and opioid-receptor ligand beta-endorphin , tyrosine receptor kinase B neurotrophic receptor expressed in neuronal and nonneuronal tissues and associated with several physiological regulations and processes such as synaptic plasticity and hyperphagia , brain-derived neurotrophic factor involved in neuronal plasticity and cognitive function and acting as modulator of neurotransmitter , kinase suppressor of Ras 2 molecular scaffold expressing majorly in brain , and tubby bipartite transcription factor were associated with obesity [ 60 — 65 ] Figure 1.

The mutations or alterations in the genes associated with obesity were linked to several clinical consequences such as the defective immune system, low blood pressure, cognitive deficiency, hypopigmentation, insulin resistance, and metabolic dysfunction [ 65 ]. Heymsfield and Wadden [ 65 ] have reviewed the pathophysiological consequences of obesity in detail. The lethal obese condition accelerates the incidence of type 2 diabetes T2D via increased adipokine, proinflammatory cytokines synthesis, and impaired insulin signaling and increased insulin resistance.

The increased lipid production in obese condition releases free fatty acids, which cause lipotoxicity and chronic diseases like T2D [ 66 ] and other disease conditions such as cirrhosis, fatty liver, steatohepatitis, stroke, and heart failure [ 67 ]. Also, the accelerated sympathetic nervous system and renin-angiotensin-aldosterone system cause systemic hypertension, which ends up with several chronic and heart diseases [ 68 ]. Due to the overweight, internal organs of obese people become damaged by mechanical stress that causes overload on joints, and increased intra-abdominal tension leads to the development of osteoarthritis and gastroesophageal reflux disease [ 69 , 70 ].

Obesity also leads to obstructive sleep apnea, which is due to the obstructions of the upper airway during sleep [ 71 ] Figure 2. GM represents densely populated microorganism such as bacteria, fungi, Archaea, protozoa, and viruses, which colonizes the human gastrointestinal tract.

Approximately trillion microbes colonize the human gut, which exhibits a symbiotic relationship with the host [ 72 ]. Each individual has unique GM composition influenced by several endogenous and exogenous factors such as gestational age, mode of delivery, breastfeeding, antibiotic exposure, diet, and lifestyle [ 73 ].

The colonization of GM is not uniform throughout the gastrointestinal tract with limited distribution in stomach and small intestine followed by a dense and diverse population in the colon due to the absence of digestive secretion, slow peristalsis, and rich nutrient supply [ 74 ]. These microbes play a significant role in maintaining host body homeostasis by participating in the digestive process and energy production, hampering pathogen colonization, and modulating the immune system.

Studies in germ-free and conventional mice showed alteration in kidney, liver, and intestinal homeostasis in germ-free mice depicting the fact that gut microbiome influences the whole body metabolism [ 75 — 77 ]. GM has received much attention related to human health and disease status in the recent decade. Conventionally, the interrelation between genetic and environmental factors such as high-calorie diet and lack of physical activity was considered as main contributor to obesity.

However, recent scientific investigations have shown that GM has emerged as a prime endogenous factor influencing obesity [ 78 , 79 ]. Emerging studies showed that prenatal gut microbiome represents the maternal microbes transmitted to the fetus through placental circulation and its composition acts as a determining factor for offspring microbial composition.

Maternal obesity during pregnancy together with GM dysbiosis reflects in offspring microbiota leading to offspring metabolic disorders.

GM of the newborn is also influenced by the factors like mode of birth, antibiotic treatment, feeding type, and sanitation [ 80 ]. In the first year of child life, the microbial composition varies according to developmental changes, host genotype, and food intake, which stabilizes similar to adult microbiota by the age of 3 years. The adult human gut is colonized by 10 14 bacteria with billions of genes exceeding the human genome content.

These microbial factories contribute to biochemical and metabolic function in the human body, which cannot be performed in its absence. In healthy adult individuals, the microbiota of the gut is in a symbiotic relationship with the host, which depends on host lifestyle, diet, and antibiotics, while in elderly people the composition of microbiota changes depending upon the alteration in digestive physiology and diet [ 81 ]. Type and density of the bacterial population in gastrointestinal GI tract depend on environmental variation such as pH, oxygen level, and nutrient availability.

Recent findings in animal and human models revealed that the GM plays a key role in nutrient acquirement, energy harvest, and host metabolic pathways, which are interrelated and are responsible for the development of obesity [ 83 , 84 ]. Healthy human GM is characterized by a high ratio of Bacteroidetes to Firmicutes, while in obese individuals inverse ratio is observed with a high prevalence of Firmicutes [ 85 ].

In addition, the elevated level of Lactobacillus species with a relatively low level of Bacteroides vulgatus was observed in obese individuals [ 86 ]. Metagenomic analysis and clinical studies on GM of lean and obese individuals exhibited diminished proportion of Bacteroidetes and increased level of Actinobacteria with no significant difference in Firmicutes revealing the fact that ratio of Firmicutes to Bacteroidetes acts as a biomarker of obesity susceptibility [ 87 , 88 ].

Mounting evidence revealed that metabolites derived by fermentation of food by GM play a vital role in regulating the host metabolism with perspective to obesity. Clostridium and Eubacterium belonging to GM convert bile acid in the intestine to its secondary forms such as deoxycholic acid and lithocholic acid which binds to TGR5 receptor G-protein-coupled receptor and stimulates the secretion of incretin hormone GLP-1 and insulin, thereby promoting the energy expenditure [ 89 ].

Long chain fatty acid such as linoleic acid derived by the GM modulates the lipid profile leading to adiposity [ 90 ]. Another important by-product of gut microbial fermentation is short chain fatty acids SCFs formed by the gut microbial digestion of indigestible poly- and oligosaccharides that escape from the digestion and absorption in the proximal jejunum [ 91 ]. SCFs primarily acetate and propionate produced by Bacteroidetes and butyrate contributed by Firmicutes regulate the host metabolism by influencing energy harvest, fat accumulation, and appetite [ 92 ].

Butyrate, the prime energy source for colonocytes, promotes proliferation and maturation of colonocytes maintaining colon healthy. In addition, butyrate protects the colon by enhancing the expression of mucin 2 and modulating immune response [ 94 ]. Acetate and propionate cross the epithelium to the liver, where the propionate gets metabolized, while acetate alone remains in the peripheral circulation [ 95 ]. SCF plays a significant role in maintaining the epithelial barrier integrity by regulating the tight junction protein claudin-1, occludin, and Zonula Occludens-1 , while downregulation of these proteins leads to translocation of bacteria and LPS triggering an inflammatory response [ 96 ].

Butyrate and propionate also reduce the appetite by i inducing the expression of leptin in adipocytes and regulating body weight and energy homeostasis by reducing food intake and increasing energy expenditure [ ] ii inducing the expression of intestinal gluconeogenesis gene promoting gluconeogenesis [ ] iii inhibiting histone acetyltransferase and deacetylases exhibiting anti-inflammatory phenotype, epigenetically inducing the immune cell proliferation and differentiation, and upregulating adiponectin mediated AMPK pathway promoting mitochondrial biogenesis and fatty acid oxidation [ ].

SCF derived from GM regulates host metabolism by interaction with complex metabolic pathways intertwined with the nervous, endocrine, and immune system. In healthy individuals SCF modulates the gut integrity, gut hormone production, and immune function, while in diseased state SCF exhibits a protective effect against diabetes, ulcerative colitis, colorectal cancer, and neurodegenerative disorders [ 94 , ]. Understanding the mechanism of interaction of SCFs with its receptor will help in exploring the therapeutic way for the treatment of obesity and health-related disorders.

The interrelation between GM and host obesity was first reported by Wostmann et al. However, the mechanism behind the report was elucidated by Jeffery Gordon and his colleagues [ 2 ] who observed an increase in total body and gonadal fat in conventional mice when compared to GF mice consuming more food. Colonization of GF mice with cecum-derived microbiota showed an increase in body fat mass together with insulin resistance, adipocyte hypertrophy, and enhanced level of circulating leptin and glucose level.

The possible mechanism involved might be 1 degradation of indigestible polysaccharide by GM increasing hepatic lipogenesis in the host and 2 suppressing intestinal expression of angiopoietin-like 4 ANGPTL4 , the inhibitor of lipoprotein lipase LPL thereby blocking the fatty acid metabolism leading to increased cellular uptake of fatty acids and adipocyte triglycerides accumulation [ 2 , , ].

GF mice fed with high fat and sugar diet exhibited lean phenotype while conventional mice fed with the same diet were observed to be obese. GF mice showed enhanced sensitivity to insulin improving glucose tolerance and exhibited altered cholesterol metabolism reducing the storage and enhancing fecal excretion of cholesterol.

GM leads to host obesity through various routes such as by altering the intestinal permeability leading to endotoxemia, enhanced calorie provision, and endocannabinoid system eCB stimulation and by regulating the lipid metabolism by enhancing lipoprotein lipase activity and lipogenesis.

Experimental studies in animals and human volunteers revealed that increased production of SCFs by GM provides additional calories to host leading weight gain [ ]. Binding of these SCFs to GPR induces the secretion of peptide hormone PYY, which reduces the intestinal transit time increasing the nutrient absorption in the intestinal lumen leading to weight gain [ ].

Feces of obese individuals showed an increased level of SCF when compared to lean individuals. Increased level of TG in adipose tissue causes hypertrophy leading to chronic inflammation, preventing further deposition of TG in adipose tissue and thereby promoting ectopic accumulation of TG in other organs developing insulin resistance [ ]. Lipopolysaccharides LPS , the cell membrane component of Gram-negative bacteria, act as triggering factors leading to low-grade chronic inflammation followed by the development of insulin resistance IR.

LPS formed in the gastrointestinal tract reach the circulation via direct diffusion by enhancing the intestinal permeability or through absorption and incorporation with chylomicron [ ].

Enhanced level of LPS in circulation is called endotoxemia where diet plays a key role. High fat intake inhibits the expression of tight junction proteins zonulin and occludin, thereby increasing intestinal permeability of LPS, the causative factor for endotoxemia. LPS interact with toll-like receptors TLR-4 in immune cells and target organs like liver and adipose tissue. Administration of Bifidobacterium infantis in mice reduced colonic permeability attenuating inflammation revealing that gut microbial composition also plays a role together with diet in altering the intestinal permeability.

Overall the studies reveal that GM activates the eCB system, which increases intestinal permeability promoting LPS migration into the circulatory system causing endotoxemia. Increased LPS, in turn, alters the tight junction integrity of the intestinal membrane enhancing increased release of LPS into circulation creating virtuous circle promoting adipogenesis. Although research on human GM has succeeded logarithmically, still this field remains a puzzle and is emerging which needs to be explored.

The gut microbiome is a complex microbial world having both beneficial and harmful microbes and manipulation of these microbes for the therapeutic purpose is possible only if the precise role of each and every individual microbe is known. GM, its metabolite, and host are interplaying systems; therefore integration of this system will give us a comprehensive idea of the function of each building block of this system [ , ].

The reduced morning systolic blood pressure was also observed in the patients of both groups treated with calorie restricted diet along with the aid of antihypertension drugs irrespective of the cheese probiotic cheese or control cheese consumption.

The urinary putrescine content and BMI changes were associated with the lactobacilli load in the intervention group. The study suggested that supplementation of probiotic cheese with a calorie restriction diet reduces the BMI and hypertension in study subjects [ 24 ]. Overweight or obese adults were supplemented with L. The results suggested that the supplementation of BNR17 reduced body weight, hip, and waist circumferences compared to the placebo group.

Gut Microbiota and Obesity

The pathophysiology of obesity and obesity-related diseases such as type 2 diabetes mellitus T2DM is complex and driven by many factors. One of the most recently identified factors in development of these metabolic pathologies is the gut microbiota. The introduction of affordable, high-throughput sequencing technologies has substantially expanded our understanding of the role of the gut microbiome in modulation of host metabolism and cardio metabolic disease development. Nevertheless, evidence for a role of the gut microbiome as a causal, driving factor in disease development mainly originates from studies in mouse models: data showing causality in humans are scarce. In this review, we will discuss the quality of evidence supporting a causal role for the gut microbiome in the development of obesity and diabetes, in particular T2DM, in humans.

Link Between Changing Gut Flora and Obesity

The pathophysiology of obesity and obesity-related diseases such as type 2 diabetes mellitus T2DM is complex and driven by many factors. One of the most recently identified factors in development of these metabolic pathologies is the gut microbiota. The introduction of affordable, high-throughput sequencing technologies has substantially expanded our understanding of the role of the gut microbiome in modulation of host metabolism and cardio metabolic disease development. Nevertheless, evidence for a role of the gut microbiome as a causal, driving factor in disease development mainly originates from studies in mouse models: data showing causality in humans are scarce. In this review, we will discuss the quality of evidence supporting a causal role for the gut microbiome in the development of obesity and diabetes, in particular T2DM, in humans.

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The majority of T2DM patients are obese. Dysbiosis in the gut microflora is strongly associated with the pathogenesis of obesity and T2DM; however, the microbiome of obese-T2DM individuals in the Pakistani population remains unexplored.

A Review on Role of Microbiome in Obesity and Antiobesity Properties of Probiotic Supplements

The journal's aim is to publish articles focused on basic, clinic care and translational research that seeks to prevent rather than treat the complications of endstage liver disease. The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two receding years. CiteScore measures average citations received per document published. Read more.

Probiotics are now recognized for several health benefits and they have been recommended as a complementary therapeutic agent for metabolic disorders. Obesity is an altered health condition, which is a resultant of irregular energy intake and energy balance, changes in gut microbiota, and improper diet with the influence of genetic makeup and environmental factors. Several studies revealed the influence of probiotic supplementation on obesity-associated consequences in vitro , in vivo , and in human clinical studies. The current manuscript discussed the factors influencing the occurrence of obesity, the interplay between microbiome and obesity, the effect of the probiotic intervention on the health status of obese people, and possible mechanism of antiobesity activity of probiotics. The literature survey revealed that the antiobese activity of probiotics might be associated with their ability to alter the intestinal microbiota, remodeling of energy metabolism, alter the expression of genes related to thermogenesis, glucose metabolism, and lipid metabolism, and change the parasympathetic nerve activity. Further intense research is necessary to figure out the best probiotic or synbiotic mixture and optimum dosage and duration of the intervention to reduce obesity and prevent the recurring of obese condition.

Gut Microbiota and Obesity: Prebiotic and Probiotic Effects

3 Comments

Jeff J.
30.01.2021 at 05:38 - Reply

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Katie R.
30.01.2021 at 19:55 - Reply

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Adriana A.
31.01.2021 at 18:09 - Reply

The evidences from animal models suggest that it is possible that the microbiota of obese subjects has higher capacity to harvest energy from the diet providing.

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