**4.1 Energy absorption**

To provide energy to their humans, obese rats consume more carbohydrates via their gut bacteria [114, 115]. When bacteria mice colonized predominantly by the obesity microbiota' did not change their food or weight, their total body fat increased in comparison to mice colonized by the Chilean biome' [88]. Obese people's gut microbiota has a larger capacity for absorbing energy from meals, according to the study. Obese mice had higher lipid uptake, according to a multi-omics study. In germ-free mice, Clostridia colonization downregulates genetic variants' fat intake [47]. In a way, the gut bacteria of fat people may produce more impact energy, leading to higher energy and weight growth. Difficult-to-digest carbohydrates are fermented by gut bacteria into short-chain fatty acids, which are either eaten or expelled in the stool. Short-chain fatty acids are necessary to maintain energy balance [116]. SCFAs have lately received a lot of attention for their positive effects on cellular integrity and lipid metabolism, although their relevance in obesity is still debatable. Intestinal permeability, metabolic disease indicators, obesity, and hypertension have all been associated with increased fecal SCFA levels [117].

#### **4.2 Central appetite and fat accumulation**

The gut microbiota has become one of the most transcription factors of intestine connection. Within the study of the morphological and molecular origins of obesity and associated illnesses, the gastrointestinal system pathway has attracted much interest. Hormonal, immunological, or neurological pathways connect both brains with the microbiome [118]. The intestinal microbiota link influences the nerve cells of said individual. The autonomic nervous system can affect the makeup and structure of the gut flora. Microbiomes affect cognitive activity in a variety of ways, including by influencing the synthesis of neuropeptides like dopamine, which are critical for gastrointestinal function regulation [119]. Lactate, a nerve terminal fuel generated by Lactobacillus and Bifidobacterium, has now been demonstrated to enhance satisfaction following a meal [120]. Protracted hunger suppression controlled via hypothalamic neurotransmitter energetic pathways can be paired with short-term stomach pleasure regulation linked with bacterial proliferation [121]. **Table 2** depicts the obesity process as part of gut flora.

In 2004, it was shown that gut microbes can influence fat accumulation [87]. The gut bacteria upregulates two key signaling pathways, glycemic reaction component binding domain or cholesterol control component related proteins, causing fat to accumulate in hepatic. Lipids directly stimulate through the liver, where they can be absorbed via visceral fat, thanks to lipoprotein lipase. Fiaf, an LPL regulator, is produced by intestinal epithelial cells. Normal mouse intestinal epithelial cells have Fiaf inhibited, allowing the host to store more energy.


**Table 2.** *Adiposity caused by gut microbes.*
