A recent study published in Scientific Reports examined the effects of nicotine exposure on host nutritional status, microbial metabolites in the gut, and metabolic homeostasis.
Study: Gut microbial metabolites show diet-dependent metabolic changes induced by nicotine administration. Image credit: Danijela Maksimovic/Shutterstock.com
The gut microbiome is associated with many physiological functions, including metabolic homeostasis. Several studies have shown that dysbiosis of the gut microbiome leads to the development of various metabolic disorders, such as type 2 diabetes.
The gut microbiota synthesizes a wide range of bioactive metabolites, which serve as messengers and indicators of microbial function.
The composition and function of these microbes are influenced by diet and daily environmental factors. The host’s metabolism is significantly influenced by metabolites synthesized by gut bacteria from food.
The fermentation of indigestible polysaccharides by gut microbes leads to the formation of short-chain fatty acids (SCFAs), which improve resistance to weight gain and insulin sensitivity.
The gut microbiota is associated with the synthesis of various fatty acid variants, promoting the host’s resistance to obesity caused by a high-fat diet (HFD).
The synthesis of fatty acid metabolites by the gut microbiota plays a crucial role in improving the host’s metabolic functions, depending on the host’s dietary environment.
Cigarette smoking is a major avoidable factor that increases mortality. The majority of smokers are susceptible to cardiovascular problems, chronic obstructive pulmonary disease (COPD), and various types of cancer.
Several studies have also indicated that exposure to secondhand smoke contributes to the development of infections caused by pathogens and worsens asthma, inflammatory bowel disease, and Crohn’s disease.
Nicotine is the primary active ingredient in tobacco. It is not only absorbed by the lung’s alveoli but is also present in the skin and gastrointestinal tract. Many positive and harmful effects of nicotine have been documented.
Due to its benefits, nicotine regulates energy intake by modulating appetite. As for its harmful effects, previous studies have documented evidence that nicotine exposure leads to the development of liver steatosis and cardiovascular diseases.
Nicotine exposure can alter the host’s metabolism by inducing changes in the gut microbiota and its metabolites.
It is imperative to understand the underlying mechanism that governs the interplay between the gut environment, microbial metabolites from food, and the metabolic homeostasis of the host under nicotine exposure.
The current study examined how nicotine exposure affects metabolic regulatory mechanisms by inducing changes in the gut microbial composition and their metabolic products.
For experimental purposes, seven-week-old male mice with comparable body weight were divided into two groups: the normal diet (ND) group and the high-fat diet (HFD) group.
These mice were exposed to nicotine or saline solution for four weeks. SCFAs and long-chain fatty acid metabolite levels were estimated after seven to eleven weeks of intervention.
The body weight of the study mice was measured once a week, and blood samples were taken for analysis.
The current study reflects the intense interplay of the gut microbiota and its metabolites, as well as the host’s metabolic phenotypes in the context of nicotine exposure.
It was found that intraperitoneal nicotine administration profoundly influences weight regulation and metabolic phenotypes, independently of reduced caloric intake.
Mechanistically, the nicotine-induced suppression of body weight was modulated by specific gut bacteria, including Lactobacillus spp., which specifically synthesized KetoB (linoleic acid) during HFD intake.
Several studies have shown that nicotine reduces body weight and food intake through the hypothalamic melanocortin system.
A decrease in the relative frequency of Lactobacillus spp. occurred in response to high HFD exposure. This bacterial population increased in the presence of nicotine, especially under HFD conditions.
The pair-feeding model in this study revealed that the main mechanism of nicotine-induced weight control is associated with reduced caloric intake. Even under ad-libitum conditions, no specific association between caloric intake and body weight was observed.
Although nicotine administration resulted in a reduction in caloric intake in both the ND and HFD groups, a more significant reduction in body weight was observed, particularly in the HFD group.
This result suggests that diet-dependent factors contribute to the weight loss induced by nicotine treatment. An increased concentration of LCFAs was observed in the HFD group, which affected the gut microbes‘ sensitivity to nicotine.
The increase in non-esterified plasma fatty acids (NEFA) after intraperitoneal nicotine administration in HFD-fed mice indicates the role of nicotine in promoting lipolysis.
The gut microbiota depletion model using antibiotic treatment in HFD-fed mice revealed that the gut microbiota and their dietary fatty acid metabolites are crucial for nicotine-induced weight loss. The treated mice also significantly reduced caloric intake after nicotine administration.
The current study identified Keto B as a regulator of nicotine-induced weight loss.
This study highlighted the broad interplay of gut microbes in response to smoking, influencing various metabolic conditions, including weight reduction. In particular, the use of microbes for weight reduction was considered in this study.