PLEASE HELP : What happens in obese mice? (Physiology)

Answer and

Explanation:

The gut microbiota has recently emerged as an important, and previously unappreciated, player in host physiology (1). In particular, the gut microbiota contributes to a variety of physiological and pathophysiological processes in the host including immune disorders (2–4), atherosclerosis (5), irritable bowel syndrome (6, 7), blood pressure regulation (8), and chronic kidney disease (9, 10). Bacteria residing in the human gut are an important component of human physiology: the total wet weight of gut microbes in the human has been estimated to be 175 g–1.5 kg (11, 12), and the cells of the microbiota outnumber human cells by 10:1 (1). These bacteria interact with the immune system of the host (13), and secrete a variety of metabolites, which enter host circulation and can affect a variety of physiological parameters (8, 14), reviewed in Ref. (15). In fact, metabolites produced by the gut microbiota have been found to play key roles in renal disease (16), blood pressure regulation (8), and immune disorders (2–4). Therefore, just as we consider the genetic background of an animal or an individual to be an important contributing factor to their physiology, so too must we consider the genetic background of the microbiota associated with that animal.

Gut microbiota vary greatly amongst laboratory animals, and these differences result in notable differences in experimental results. Mice of the same strain from different vendors have different microbiota profiles (17), and similarly, the same mice housed at different institutions have different microbiota profiles (18, 19). Conversely, inoculating two different inbred mouse strains with the same gut bacteria leads to differences in host gene expression between the two mouse strains (20). Clearly, there is a complex interplay between the genetics of the microbiota and that of the host organism, which has only recently begun to be appreciated.

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Gut Microbiota as an Experimental Parameter

Examples in the literature have highlighted the important and unexpected ways in which gut microbiota can affect a variety of experimental parameters. In a series of studies, Vijay-Kumar et al. (13, 21) reported that although TLR5 null animals initially had a colitis phenotype, when these mice were “rederived” and their gut microbiota altered, the colitis phenotype was greatly attenuated, and instead the null animals exhibited metabolic syndrome. In addition, Lathrop et al. put forward a model by which T-cells are educated not only by self/non-self mechanisms, but also by microbiota-derived “non-self” antigens (22). Accordingly, they found that the presence or absence of microbiota determined whether T cells would induce colitis in mice. Finally, Yang et al. reported that when the same knockout mice were housed at two different institutions, they had markedly different microbiota profiles – and the mice at one institution (MIT) were quite susceptible to colitis, whereas mice at the other institution (MHH) failed to develop any significant pathology under the same conditions (19). Unequivocally, altering gut microbiota – even by housing animals at different institutions – can have dramatic effects on the phenotype observed.

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Gut Microbiota and Obesity and Diabetes

It is important to note that not only can microbiota affect host physiology, but the gut microbiota are not necessarily stable over time. Rather, gut microbiota can change or shift as a result of experimental manipulation (in animals) or changes in lifestyle or nutrition (in humans). It is now appreciated that there are “shifts” in microbiota that occur in obesity in mice, rats, and humans (23–26). In one study, Turnbaugh et al. (25) examined human female twin pairs concordant for leanness or obesity, and found that obesity was associated with phylum-level changes in microbiota.

it is the second option.

that tool is called an altimeter which measures your altitude which can be used to tell which atmosphere you are currently in, including the stratosphere.

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