High fat diet have been know to alter the gut microbiota. it elevates gram negative microorganisms which elevates the metabolic disorder and insulin resistance

It seems that there is a cicardian rythm (biological clock) in everything. The challenge is to distinguish how it works in every one of us and to fine tune our "clocks" (personalized medicine) in order to achieve longevity, and quality of life.

Most microbiologists would say yes! The microbiota is made up of fast and slow growers. Restricting feeding times would have an impact on the fast growers especially.

Since I am not a microbiologist I would offer an alternate view considering restricted feeding times. Before nutrients get into the gut for microflora action [in the lower gut], there are more plausible mechanisms for metabolic disarray occurring earlier [prandial absorption]. Delayed glucose or triglyceride clearance in blood come from meal overloads in humans, akin to a pro-inflammatory state. Both Glycemic Index and the nature of fatty acids can be contributory independent of a healthy fit person. So for those persons with diabetes or metabolic syndrome these effects can be enhanced.

Since I am not a microbiologist I would offer an alternate view considering restricted feeding times. Before nutrients get into the gut for microflora action [in the lower gut], there are more plausible mechanisms for metabolic disarray occurring earlier [prandial absorption]. Delayed glucose or triglyceride clearance in blood come from meal overloads in humans, akin to a pro-inflammatory state. Both Glycemic Index and the nature of fatty acids can be contributory independent of a healthy fit person. So for those persons with diabetes or metabolic syndrome these effects can be enhanced. I am uploading the nature of discussion by 2 stalwarts of metabolic syndrome Grundy and Reaven], an epidemiological paper on risk of diabetes as per GI loading in the EPIC Study and finally a paper on triglyceride structure and health risk which sort of explains the digestive process and uptake of dietary fatty acids. These papers will be continuously uploaded in the following posts.

Since I am not a microbiologist I would offer an alternate view considering restricted feeding times. Before nutrients get into the gut for microflora action [in the lower gut], there are more plausible mechanisms for metabolic disarray occurring earlier [prandial absorption]. Delayed glucose or triglyceride clearance in blood come from meal overloads in humans, akin to a pro-inflammatory state. Both Glycemic Index and the nature of fatty acids can be contributory independent of a healthy fit person. So for those persons with diabetes or metabolic syndrome these effects can be enhanced.

Your hypothesis linking the effects of time restricting feeding to gut microbiota is really interesting. I completely agree with Verlaine Timms : time restricting feeding will definitilety have an impact on gut microbiota. But is it responsible for the effects you mentioned (even partially) ? I have no idea. It would be posible to test it by transplanting this "time restrictig feeding microbiota" to germfree mice and see if it has an effect on obesity development

A comparison of the total microbiota between the two groups would help to answer the question. The microbiota between healthy and obese individuals is different with the latter changing once the diet is changed to a healthier one. See the attachment for a good review.

I like the idea Philippe, of doing a transplant into germ free mice because it bypasses the complexity of trying to analyze the mice microbiota when we still know so little about the relevance and effect of the different strains.

also-

"Gut Bacteria Linked to Obesity and Metabolic Syndrome Identified"

good quick summary of a study that found it wasnt the dominant bacteria genuses that correlated with metabolic disease in an Amish population but differing levels of 26 other strains.

http://www.sciencedaily.com/releases/2012/08/120815174902.htm

hello. when you use a food restricted schedule, have mani changes in the liver. the liver process, stores, metabolized and more activities about the food. you can review this articles: good luck. Persistence of metabolic rhythmicity during fasting and its entrainment by restricted feeding schedules in rats. and

Anticipatory changes in liver metabolism and entrainment of insulin, glucagon, and corticosterone in food-restricted rats

Dear fellows,

I believe a good idea would be to identify differences in flora of gut between obese and normal individuals. I believe that it would be more interesting to let the bacteria themselves to do the job.

The lab group I work with focuses on the mechanisms of obesity and type 2 diabetes, so this area of research is of interest to me. Quite a bit of research has already been conducted on this topic and there seems to be a link between high fat feeding and altered gut microbiota; this condition is commonly referred to as metabolic endotoxemia. Additionally, there is evidence that altered gut microflora can affect the endocannabinoid system tone. This increases the permeability of the intestines and results in an increase in circulating LPS, contributing to low-grade chronic inflammation. Upon analysis of the cecal contents of high fat and control diet mice, P.D. Cani et. al. found significant reductions in the Bifidobacterium, Clostridium, and Bacteroides spp. populations in high-fat fed mice. Attached is a review article by the same author.

Hi Lauren,

That is interesting the endocannabinoid system is involved, given its additional role in stimulating hunger.

Do you think there could be a feedback mechanism where the obesity-inducing bacteria in the gut trigger hunger in the host, ensuring the high fat diet is continued and the environment in the gut remains conducive to their survival?

So once the microbiota is altered and these bacteria take hold, they use all their evolutionary tactics to keep the microbiota balanced in their favour.

Basically, by giving the host the munchies!

I believe scientists are currently targeting endocannabinoid receptors as a way of controlling hunger and aiding weight loss, but that may have nothing to do with the localized affects you have observed near the gut?

In any case, thank you for your input

I have not personally conducted the research, I'm just reporting what I've read from other labs conducting obesity research. :)

It is my understanding that the eCB receptors in the colon are responsible for gut permeability. According to available data by G.G. Muccioli et. al., blockade of CB1 receptors protects against weight gain and reduces energy intake. However, high fat diet appears to result in a decrease in the total numbers of gram-positive bacteria and since LPS, a component of gram-negative bacteria, stimulates eCB production, this would result in an increase in CB1 expression in the colon, increased gut permeability and increased infiltration of LPS into the plasma and other tissues, like muscle and adipose; all of which can be reduced using CB1 receptor antagonists.

LPS impairs the differentiation of preadipocytes to mature adipocytes, causing existing mature adipocytes to store more lipid and become hypertrophic. Enlarged adipocytes secrete greater amounts of leptin which, under normal conditions, would reduce appetite. Under conditions of hyperphagia induced obesity and prolonged hyperleptinemia, these individuals would develop leptin resistance and might always feel hungry, contributing to increased energy intake. All this together implies a feedback loop between the gut and the adipose which could drive the expansion and inflammation of the adipose, resulting in obesity and, eventually, insulin resistance.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925525/