Obesity, a condition characterized by a body mass index (BMI) over 30 kg/m², is a major global health concern. It significantly increases mortality risk and is a key risk factor for diseases like diabetes, hypertension, heart disease, stroke, and even cancer. The causes of obesity are complex, involving environmental, genetic, neural, and endocrine factors. Recent research has also highlighted the role of the gut microbiota in obesity, with specific bacterial profiles being associated with both obesity and leanness.
The Link Between Diet, Gut Microbiota, and Obesity
Recent epidemiological studies point to a connection between dietary habits, gut microbiota, and weight. Eating ‘fast food’ items such as potato chips increased likelihood of obesity, whereas eating yogurt prevented age-associated weight gain in humans. It's well-documented that "fast food," high in fat and salt but low in fiber and essential vitamins, is a major contributor to the obesity epidemic in Western societies. Conversely, recent research suggests that yogurt consumption can prevent age-associated weight gain, though the exact mechanisms remain unclear.
The Role of the Immune System
Experimental data suggests that the white adipose tissue of obese organisms is in a low-grade, persistent state of chronic inflammation that exerts adverse systemic effects. The most prominent inflammatory cell type of the obesity-associated inflammation is the adipose tissue macrophage. Macrophages are recruited and surround dead adipocytes, thus creating the so-called crown-like structures (CLS). These cells along with hypertrophic adipocytes are thought to be the key cells initiating the unique subclinical pro-inflammatory signaling cascade encountered in obesity. Macrophages, B and T lymphocytes, and up-regulated pro-inflammatory cytokines including TNF-α, IL-1, IL-6, IL-17, and monocyte chemoattractant protein-1 (MCP-1) have been reported to contribute to obesity-associated pathologies.
Lactobacillus Reuteri: A Potential Ally in Weight Management
Given the potential role of gut microbiota in weight management, researchers have explored the effects of probiotics, live microorganisms that, when administered in adequate amounts, confer a health benefit on the host. Dietary probiotic consumption alters gut microbiota and may be an effective strategy not only for weight loss but also for preventing weight regain after loss. One such probiotic, Lactobacillus reuteri ( L. reuteri), has shown promising results in preclinical studies.
L. Reuteri and its Impact on Fat Accumulation
In a mouse model of obesity, purified probiotic organisms alone prevented weight gain, and these protective effects were irrespective of the baseline diet. This effect could be isolated to a single purified probiotic microbe, namely Lactobacillus reuteri. Abdominal fat (Fig. 2a) and subcutaneous fat (Fig. 2b) accumulations were significantly reduced in Swiss mice eating purified L. reuteri in combination with either control or Western diet (Fig. 2a-c). Specifically, the abdominal (epididymal) fat mass is significantly reduced in probiotic-consuming Swiss mice (a). The slenderizing effect of L. reuteri is also observed in the subcutaneous fat depot. The subcutaneous fat layer (SF) is significantly thicker and has many CLS (inset) in “fast food”-fed mice in contrast to mice eating the same diet and L. reuteri. There is thicker dermis and increased subcutaneous hair follicle profiles in the left inset of the “fast food”+probiotic skin image (b). Fad pad weight and subcutaneous fat thickness histomorphometric analyses show that probiotics protect from age-associated obesity irrespective of baseline diet (c). Eating probiotics benefits aged Swiss mice as well as the young animals, evident here from the body weight analysis of 7- and 9-months-old male and female mice (d). Skin histology: Hematoxylin and eosin, Bars = 250 µm.
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L. Reuteri's Mechanism of Action: Immune Modulation
Importantly, eating L. reuteri bacteria acted without changing the existing gastrointestinal (GI) microbial composition in stool or level of calorie consumption; instead, the slenderizing microbial mechanism involved bacteria-triggered changes in the host immune system composition. The effect was in particular dependent on CD4+ T cells and the presence of anti-inflammatory Il-10, as Il-10 deficient animals were resistant to L. reuteri-induced effects. Adoptive transfer of purified Il-10-competent L. reuteri-induced Foxp3+ Treg cells was sufficient to rescue fat pathology and lessen body fat in naïve recipient animals.
It is well established that intestinal microbes modulate host health through activities of CD4+ T cells [21]-[22], at least in part through Il-6-dependent reciprocal functions of anti-inflammatory Foxp3+ Treg cells and pro-inflammatory Th17 cells [6], [23]. Thus, we examined T cell subpopulations and found that obese mice eating Western chow had increased frequencies of Il-17 expressing cells which is in line with a previous report [6] (Fig. 1b and 1d). Importantly, when examining peripheral blood of human subjects frequently dining on ‘fast food’ we found a similar pro-inflammatory Th17-biased profile (Fig.
Recognizing that eating probiotics made mice thin without restructuring their microbial communities or reducing food intake, we hypothesized that probiotic organisms may protect from obesity by up-regulating anti-inflammatory immune activities; in particular, levels of anti-inflammatory cytokine IL-10. This reasoning was based upon data that interleukin-10 is pivotal in mounting immune tolerance to microbes along intestinal mucosal interfaces [25]-[26]. In support of this concept, it was found that the Swiss mice eating L. reuteri exhibited higher levels of IL-10 protein in serum than matched control mice (Fig. 1d).
L. Reuteri and Gut Microbiome Diversity
Although probiotics didn’t restructure resident microbiota communities, a pre-existing diverse microbial community was required for optimal slenderizing effects as illustrated by the fact that mice raised under germ-free conditions, and then fed L reuteri under general housing conditions, fail to benefit from eating probiotic organisms (Fig.
Human Studies and the Potential for Translation
Recent epidemiological research shows eating “yogurt” prevents age-associated weight gain in humans [1]. Humans frequently eating ‘fast food’ also show an elevated ratio of pro-inflammatory IL17+/anti-inflammatory Foxp3+ Treg in peripheral blood cells compared to subjects never eating ‘fast food’ (e). Probiotic-consuming slim mice chose similar calories when compared with obese animals, regardless of baseline diet, highlighting potential for translational medicine (f).
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Further Research and Considerations
While the findings regarding L. reuteri and weight loss are promising, it's important to acknowledge that much of the research is currently in preclinical stages. More research is needed to fully understand the mechanisms of action and to determine the optimal dosage and delivery methods for human consumption.
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