The human body is home to trillions of bacteria communities, outnumbering all our cells by a factor of ten. Despite their minuscule size, these bacteria collectively weigh about 2-3 kg. Anatomically, they are present in the esophagus and stomach in smaller numbers, increasing from the small intestine to the large intestine, with the highest concentration found in the colon. The community of bacteria that coexist with us in our bodies is referred to as the microbiota, and the genetic content of these bacteria is known as the microbiome. The gut microbiota has effects on nutrition, immunity, behavior, and certain chronic diseases. It functions as a metabolic, endocrine, and immunological organ.
The gut microbiota establishes a symbiotic relationship by performing certain functions that the human body cannot accomplish. It aids in the digestion of indigestible foods, synthesizes some vitamins and micronutrients, detoxifies dietary toxins and carcinogens, contributes to the recycling of cholesterol and bile acids, supports the health of intestinal cells, regulates intestinal blood flow, and prevents the proliferation of harmful bacteria in the gut. The intestines are the regions where bacteria are most densely populated. The development of the gut microbiota begins while in the womb. During birth (especially in vaginal deliveries) and breastfeeding, infants continue to acquire bacteria. Over time, a unique microbiota develops for almost every individual. The composition of this microbiota is shaped by factors such as the mode of delivery (vaginal or cesarean), antibiotic treatments, nutrition (breast milk or formula), and environmental influences. By around three years of age, the gut microbiota is largely established and remains relatively stable throughout adulthood. However, changes can occur with aging due to alterations in digestive physiology and diet.
The gut microbiota is easily influenced by diet, medications, and dietary factors, and even a single dose of antibiotics can cause changes in the microbiota. There are many causes for the development of obesity, and the process is not fully understood. The differences in microbiota between obese and lean individuals suggest that the microbiota may have an effect on obesity. It is now known that gut microbiota is associated with obesity. The relationship between gut microbiota and obesity was first demonstrated in studies using germ-free animals raised in controlled environments. Germ-free rodents were observed to require 30% more food than normal individuals to maintain their body weight. Despite consuming more food, germ-free mice had 40-45% less body fat compared to normal mice. When germ-free mice were given microbiota transplants from normal mice, about a 60% increase in body fat was observed within two weeks, accompanied by insulin resistance, hypertrophy of fat cells, and increased levels of leptin and glucose in the blood.
Interestingly, germ-free mice were found not to become obese when fed a diet rich in sugars and fats. These findings demonstrated that gut microbiota is related to obesity. This phenomenon can be explained by the contribution of gut microbiota to the digestion of indigestible foods, thereby increasing energy efficiency.
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