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Microbiota and Obesity: Comparison
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Please note this is a comparison between Version 2 by Conner Chen and Version 1 by Carlos Rosales.

Body weight is influenced not only by the quality of the diet and the amount of physical activity, but also by work schedules, ambient temperature, lack of sleep; drugs that modify endocrine and reproductive functions, gut microbiota, and epigenetic effects.

  • Microbiota
  • Obesity

1. Introduction

Obesity is a clinical condition defined as a lopsided body weight associated with an exaggerated enlargement of the adipose tissue [1,2][1][2]. In simple terms, obesity appears when people have low physical activity (a sedentary lifestyle) and increased ingestion of food, particularly of high-energy-yielding groceries [3]. However, obesity is more complex than an imbalance between caloric intake and energy requirements. External factors, such as genetics, socioeconomic status, and environment, influence food consumption, nutrient assimilation, thermogenesis, and fat storage in various adipose tissues [4]. At the present time, 39% of the world population is obese or overweight. The prevalence of these conditions has steadily increased globally during the last 30 years [5], and it is expected that, if this tendency continues, by 2025, obesity prevalence in the world will be 18% in men and 21% in women [6]. This tendency makes obesity the 21st century epidemic [7,8][7][8] with an important economic burden on health costs because obesity is associated with the development of multiple pathological conditions also known as obesity-related complications, including type 2 diabetes mellitus, cardiovascular diseases, some types of cancer, and coronavirus disease 2019 (COVID-19) [3,9,10,11][3][9][10][11].
Obesity is also characterized by a mild, chronic, systemic inflammation. The excessive accumulation of fat in the adipose tissue is due to either an increase in adipocyte size (hypertrophy) or the growth of new adipocytes (hyperplasia). Both conditions cause adipocyte stress and malfunction leading to inflammation [12]. As obesity worsens, the initial mild (low-grade) inflammation becomes chronic, and later it turns systemic [13,14,15][13][14][15]. The adipose tissue is composed not only of adipocytes (mature fat cells), but also of different types of immune cells, which are important for tissue homeostasis [16,17][16][17]. During obesity, stressed adipocytes produce adipokines, which recruit and activate innate immune cells [18]. These immune cells in turn perpetuate the inflammation state via production of cytokines and chemokines that can even influence other parts of the body, creating a systemic inflammatory condition [19,20][19][20].
The vast majority of immune cells infiltrating the adipose tissue are macrophages [21,22][21][22]. These immune cells accumulate around adipocytes in crown-like structures [23] where macrophages can proliferate and further maintain the adipose tissue inflammation [24]. However, recently it has become evident that neutrophils, the most abundant leukocytes in blood and the primary effector cells of acute inflammation, are also the first immune cells infiltrating the adipose tissue [25]. Neutrophils then get activated [26,27,28][26][27][28] and release multiple inflammatory factors and chemokines that recruit macrophages and other immune cells including B cells, T cells, and NK cells [29]. The crosstalk between adipocytes and neutrophils further promotes the adipose tissue inflammation [30].

2. Obesity

Obesity is associated not only with an excessive accumulation of fat in the adipose tissue [1,2][1][2], but also with a mild, chronic, systemic inflammation [12]. Increased fat accumulation results from an imbalance between the energy derived from food ingestion and the energy used for body functions. However, this simple view (based on thermodynamics) does not take into consideration the complexity of body weight control. Body weight is influenced not only by the quality of the diet and the amount of physical activity, but also by work schedules, ambient temperature, lack of sleep; drugs that modify endocrine and reproductive functions, gut microbiota, and epigenetic effects [4]. The complexity of weight control makes the etiology of obesity an intricate mix of personal choices, socioeconomic level, and environmental factors [2]. As a result, obesity has become a pandemic health problem [7,8][7][8]. In 2016, the World Health Organization (WHO) estimated that more than 1.9 billion people, 18 years and older, were overweight. Of these, over 650 million were obese. In addition, over 340 million children and adolescents aged 5–19 were also overweight or obese [31]. Assessment of obesity is not easy since there are multiple ways to accumulate fat in tissues. This variation creates two principal types of obesity: subcutaneous and visceral. In subcutaneous obesity (which is more common in women), excess fat is found under the skin surrounding the hip and thigh areas, while in visceral obesity (which is more common in men), fat is concentrated in the abdominal region, primarily in the mesenteric adipose tissue. In order to assess obesity, several indicators have been used. The body mass index (BMI) is one such indicator that estimates overweight and obesity based on the weight of the individual expressed in kilograms (kg) divided by the square height of the individual in meters (m2) [31]. In addition, other indicators besides the BMI should be considered to fully assess the severity of obesity. For example, waist circumference helps to discriminate between subcutaneous obesity and visceral obesity, and it is a good indicator of poor health. A strong correlation of waist circumference with all-cause mortality was found for men (with waist circumferences larger than 110 cm) and for women (with waist circumferences larger than 95 cm) [32]. Obese individuals are at a greater risk of developing numerous health problems that play a role in premature death [5,31,32][5][31][32], including features of the metabolic syndrome [1[1][33],33], and other obesity-related complications such as type 2 diabetes mellitus, cardiovascular diseases, some types of cancer [3], and COVID-19 [11]. In addition, obesity has a negative influence on psychological and cognitive functions [34,35][34][35].

3. Microbiota and Obesity

Obesity is usually accompanied by a mild, chronic, systemic inflammation. This inflammatory state is initiated by damage to the adipose tissue due to excessive fat deposition, and also by increased intestinal permeability due to alterations to the gut microbiota [36]. The gut microbiota is the community of microorganisms (including bacteria, archaea, fungi, protozoa, and viruses) that reside in the digestive tract. The dominant phyla in the gut are Firmicutes (Gram-positive) (60–65%), Bacteroidetes (Gram-negative) (20–25%), Proteobacteria (such as Escherichia and Enterobacteriaceae) (10%), and Actinobacteria (Gram-positive) (3%) [37,38][37][38]. Recent years have seen an increasing evidence of the association of changes in gut microbiota with the development of obesity (reviewed in [39,40,41,42,43][39][40][41][42][43]). This association was evidenced through initial reports showing that germ-free mice fed a high-fat diet had reduced body fat and did not develop obesity [44,45][44][45]. However, these mice recuperated fat and developed insulin resistance and glucose intolerance after reconstitution with the gut microbiota from normal mice [45]. Then, a metagenomic analysis showed that the two main bacterial phyla, Firmicutes and Bacteroidetes [37], maintain a relatively constant balance both in lean mice and humans; but in obese individuals, higher levels of Firmicutes and lower levels of Bacteroidetes were found [46,47][46][47]. Interestingly, after eliminating the high-fat diet, the ratio of Firmicutes/Bacteroidetes was reverted to the levels found in lean individuals [46]. Most other studies have had similar results [40]. However, numerous reports of opposite results suggest that the Firmicutes/Bacteroidetes ratio not always increases in obesity, and thus, further studies are required to resolve this issue [48]. Nevertheless, it seems that changes in specific bacteria, more than the ratio of the phyla, are better associated with obesity [49]. Altering the gut microbiota composition has important metabolic consequences. For example, obesity-associated microbiotas have been found to be more efficient at obtaining energy from the diet by producing enzymes that degrade food more efficiently, thus favoring a larger caloric intake [47]. Another significant consequence of an altered microbiota during obesity is the increased intestinal permeability [50], which leads to the escape of bacteria and bacterial products across the intestinal barrier into the blood circulation [36]. A major bacterial product found to cross the intestinal barrier in obese individuals is lipopolysaccharide (LPS), which triggers innate immune cells, leading to inflammation [51,52][51][52]. A high-fat diet increases the growth of Gram-negative bacteria and promotes LPS absorption across the intestinal barrier [51,53][51][53]. Thus, LPS absorption caused by ingestion of high-fat diets is related to obesity-induced low-grade systemic inflammation [54]. In contrast, other bacterial products such as short-chain fatty acids (SCFAs) have been associated with maintenance of reduced weight [55]. SCFAs, predominantly butyrate, acetate, and propionate, are produced by fermentation of nondigestible carbohydrates (dietary fiber) by various gut bacteria [56] and serve as an energy source for the colonic epithelia (butyrate), liver (propionate), and peripheral tissues (acetate) [57]. In particular, butyrate and propionate induce the production of gut hormones, such as hormone peptide tyrosine (PYY) and glucagon-like peptide-1 (GLP-1) from colonic L cells [58] via their cognate free fatty acid receptors (FFARs) [59]. In this way, SCFAs lead to reduced food intake, resulting in weight loss and the maintenance of reduced weight [50,59,60][50][59][60]. In addition, SCFAs can diminish inflammation by modulating several leukocyte functions, including reduced production of inflammatory cytokines and eicosanoids, inhibition of leukocyte migration to inflammation sites [61], and induction of neutrophil apoptosis [62]. Based on the evidence that microbiota composition can modulate body weight and inflammation, a growing interest exists to modify the gut microbiota by different approaches. The use of probiotics (live microorganisms which in proper quantities could provide a health benefit) or of prebiotics (nondigestible food ingredients that favor growth of health-promoting bacteria) has been extensively tried [63,64,65][63][64][65]. Furthermore, fecal microbiota transplantation is now considered as a feasible therapy for treating obesity by influencing the composition of the gut microbiota [66]. Although some reports suggest that these approaches can reduce obesity and other associated complications [41[41][67],67], in general, only a limited success is achieved by microbiota-related interventions for body weight control in humans [68]. Therefore, future research is needed combining different approaches to improve the beneficial effects of microbiota modification on obesity. Nevertheless, it is clear that an altered microbiota during obesity can induce a low-grade systemic inflammation by increasing intestinal permeability [50] and allowing bacterial products, such as LPS, to cross the intestinal barrier into the blood circulation [36].

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