Fructose rapid bacterial fermentation

[SamYo123]

How would you "fix" something like this?

And how would you "fix" fructose malabsorption ?

Edit found this

High sucrose diet-induced dysbiosis of gut microbiota promotes fatty liver and hyperlipidemia in rats - PubMed

Excess sucrose intake has been found to be a major factor in the development of metabolic syndrome, especially in promoting nonalcoholic fatty liver disease. The excess fructose is believed to targets the liver to promote de novo lipogenesis, as described in major biochemistry textbooks. On the...

pubmed.ncbi.nlm.nih.gov

explains alot

 

[UG Krishnamurti]

"Wistar male rats were fed either a control starch diet or a high-sucrose diet for 4 weeks."

I would personally like to know what kind of diet that was. "High sucrose" doesn't mean it's not also "high fat". That combination would sure cause problem due to the Randle Cycle metabolic process and inability of the body to use sugar efficiently.

 

[Elie]

"Wistar male rats were fed either a control starch diet or a high-sucrose diet for 4 weeks."

I would personally like to know what kind of diet that was. "High sucrose" doesn't mean it's not also "high fat". That combination would sure cause problem due to the Randle Cycle metabolic process and inability of the body to use sugar efficiently.

2. Materials and methods 2.1. Experimental animals The animal studies were approved by the Animal Research Committee of the Center for Animal Research and Education, Nagoya University, Japan (permit numbers: 2015052901 and 2018051101). The experiments were performed according to the guidelines stipulated by this committee. Wherever possible, efforts were made to minimize animal suffering. For the experiments on the architecture of gut microbiota, 40 5-week-old male Wistar rats purchased from SLC (Shizuoka, Japan), weighing approximately 90 g each, were independently housed under a 12 h light-12 h dark cycle (lights on 0800-2000) at an average temperature of 23 ± 1°C, with free access to water. After a 6-day acclimatization period, each rat was assigned to one of two groups (n = 20 for each group), i.e. fed either a control starch diet (CSD) or a HSD ad libitum for 4 weeks, with the equivalent initial body weights and plasma triglyceride concentrations. Either diet consisted of 65.3 g carbohydrate (only starch or sucrose), 20 g casein, 5 g cellulose, 5 g corn oil, 3.5 g mineral mixture [27], 1 g vitamin mixture [27], and 0.2 g choline chloride for each 100 g, as described previously [28]. For experiments investigating the antibiotic treatment, 24 5-week-old male Wistar rats were housed under the same conditions as the conventional experiment. They were assigned to four groups (n = 6 for each group) after a weeklong acclimatization period, and then, fed with either CSD or HSD ad libitum for 4 weeks, as described above, with or without antibiotic treatment. Antibiotics were delivered to the treated rats in a cocktail of ampicillin (1 g/L), metronidazole (1 g/L), neomycin (1 g/L), and vancomycin (500 mg/L) [29,30] in their drinking water for the entire duration of the experiment. A fresh antibiotic cocktail was supplied every day. All antibiotics were purchased from Sigma Aldrich (St. Louis, MO, USA). Body weight and food intake of the rats were measured every day. Rats were sacrificed by decapitation without anesthesia at ZT2 (Zeitgeber time, ZT0 is defined as the point of lights on), ZT8, ZT14, ZT18, and ZT22 (n = 4 for each group at each time point) from day 28 to day 29 for the experimental study on cecal gene expression. For the antibiotic treatment experiment, rats were sacrificed at ZT2. The samples of the blood, liver, cecal mucous membranes, and cecal contents were harvested and frozen immediately in liquid nitrogen. Samples were stored at −80°C until further analysis.

 

[UG Krishnamurti]

2. Materials and methods 2.1. Experimental animals The animal studies were approved by the Animal Research Committee of the Center for Animal Research and Education, Nagoya University, Japan (permit numbers: 2015052901 and 2018051101). The experiments were performed according to the guidelines stipulated by this committee. Wherever possible, efforts were made to minimize animal suffering. For the experiments on the architecture of gut microbiota, 40 5-week-old male Wistar rats purchased from SLC (Shizuoka, Japan), weighing approximately 90 g each, were independently housed under a 12 h light-12 h dark cycle (lights on 0800-2000) at an average temperature of 23 ± 1°C, with free access to water. After a 6-day acclimatization period, each rat was assigned to one of two groups (n = 20 for each group), i.e. fed either a control starch diet (CSD) or a HSD ad libitum for 4 weeks, with the equivalent initial body weights and plasma triglyceride concentrations. Either diet consisted of 65.3 g carbohydrate (only starch or sucrose), 20 g casein, 5 g cellulose, 5 g corn oil, 3.5 g mineral mixture [27], 1 g vitamin mixture [27], and 0.2 g choline chloride for each 100 g, as described previously [28]. For experiments investigating the antibiotic treatment, 24 5-week-old male Wistar rats were housed under the same conditions as the conventional experiment. They were assigned to four groups (n = 6 for each group) after a weeklong acclimatization period, and then, fed with either CSD or HSD ad libitum for 4 weeks, as described above, with or without antibiotic treatment. Antibiotics were delivered to the treated rats in a cocktail of ampicillin (1 g/L), metronidazole (1 g/L), neomycin (1 g/L), and vancomycin (500 mg/L) [29,30] in their drinking water for the entire duration of the experiment. A fresh antibiotic cocktail was supplied every day. All antibiotics were purchased from Sigma Aldrich (St. Louis, MO, USA). Body weight and food intake of the rats were measured every day. Rats were sacrificed by decapitation without anesthesia at ZT2 (Zeitgeber time, ZT0 is defined as the point of lights on), ZT8, ZT14, ZT18, and ZT22 (n = 4 for each group at each time point) from day 28 to day 29 for the experimental study on cecal gene expression. For the antibiotic treatment experiment, rats were sacrificed at ZT2. The samples of the blood, liver, cecal mucous membranes, and cecal contents were harvested and frozen immediately in liquid nitrogen. Samples were stored at −80°C until further analysis.

Thanks.

What do you think is the equivalent of 5g corn oil in a human body on a daily basis.

 

[Elie]

Multiply by the ratio between human and rat weight?
thing is both groups consumed corn oil.
Perhaps there is something about rat physiology that might favor starch.
I don't know.

 

[Vins7]

S

"Wistar male rats were fed either a control starch diet or a high-sucrose diet for 4 weeks."

I would personally like to know what kind of diet that was. "High sucrose" doesn't mean it's not also "high fat". That combination would sure cause problem due to the Randle Cycle metabolic process and inability of the body to use sugar efficiently.

So, what is a good sugar fat ratio or macronutrient distribution for not affecting Randle Cycle?
Is really Randle Cycle an important aspect? I think once Ray recommended a macro distribution like 40/30/30 C/P/F, I'm not sure.

 

[Hans]

How would you "fix" something like this?

And how would you "fix" fructose malabsorption ?

Edit found this

High sucrose diet-induced dysbiosis of gut microbiota promotes fatty liver and hyperlipidemia in rats - PubMed

Excess sucrose intake has been found to be a major factor in the development of metabolic syndrome, especially in promoting nonalcoholic fatty liver disease. The excess fructose is believed to targets the liver to promote de novo lipogenesis, as described in major biochemistry textbooks. On the...

pubmed.ncbi.nlm.nih.gov

explains alot

It's best to throw animal studies out the window. Human study:

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases

High consumption of fructose and high-fructose corn syrup is related to the development of obesity-associated metabolic diseases, which have become the most relevant diet-induced diseases. However, the influences of a high-fructose diet on gut microbiota ...

www.ncbi.nlm.nih.gov

"High-fructose intake by HFS causes a reduction of beneficial butyrate producing bacteria and a gut microbiota profile that may affect unfavorably host lipid metabolism whereas high consumption of fructose from fruit seems to modulate the composition of the gut microbiota in a beneficial way supporting digestive health and counteracting harmful effects of excessive fructose."

This study is only 14 days long, but it's still worth a look, because the microbiome can shift in 24 hours and start to cause issues:

Excess dietary fructose does not alter gut microbiota or permeability in humans: A pilot randomized controlled study - PubMed

In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD.

pubmed.ncbi.nlm.nih.gov

"Results: Routine blood, uric acid, liver function, and lipid measurements were unaffected by the fructose intervention. The fecal microbiome (including Akkermansia muciniphilia), fecal metabolites, gut permeability, indices of endotoxemia, gut damage or inflammation, and plasma metabolites were essentially unchanged by either intervention.
Conclusions: In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD."

 

[SamYo123]

It's best to throw animal studies out the window. Human study:

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases

High consumption of fructose and high-fructose corn syrup is related to the development of obesity-associated metabolic diseases, which have become the most relevant diet-induced diseases. However, the influences of a high-fructose diet on gut microbiota ...

www.ncbi.nlm.nih.gov

"High-fructose intake by HFS causes a reduction of beneficial butyrate producing bacteria and a gut microbiota profile that may affect unfavorably host lipid metabolism whereas high consumption of fructose from fruit seems to modulate the composition of the gut microbiota in a beneficial way supporting digestive health and counteracting harmful effects of excessive fructose."

This study is only 14 days long, but it's still worth a look, because the microbiome can shift in 24 hours and start to cause issues:

Excess dietary fructose does not alter gut microbiota or permeability in humans: A pilot randomized controlled study - PubMed

In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD.

pubmed.ncbi.nlm.nih.gov

"Results: Routine blood, uric acid, liver function, and lipid measurements were unaffected by the fructose intervention. The fecal microbiome (including Akkermansia muciniphilia), fecal metabolites, gut permeability, indices of endotoxemia, gut damage or inflammation, and plasma metabolites were essentially unchanged by either intervention.
Conclusions: In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD."

Doesnt, the sucrose affect B vitamins, and so affect the microbiome?

 

[Hans]

Doesnt, the sucrose affect B vitamins, and so affect the microbiome?

Minimally. Depending on the dose ofc.

 

[SamYo123]

Minimally. Depending on the dose ofc.

200-300g a day?

 

[jet9]

It's best to throw animal studies out the window. Human study:

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases

High consumption of fructose and high-fructose corn syrup is related to the development of obesity-associated metabolic diseases, which have become the most relevant diet-induced diseases. However, the influences of a high-fructose diet on gut microbiota ...

www.ncbi.nlm.nih.gov

"High-fructose intake by HFS causes a reduction of beneficial butyrate producing bacteria and a gut microbiota profile that may affect unfavorably host lipid metabolism whereas high consumption of fructose from fruit seems to modulate the composition of the gut microbiota in a beneficial way supporting digestive health and counteracting harmful effects of excessive fructose."

This study is only 14 days long, but it's still worth a look, because the microbiome can shift in 24 hours and start to cause issues:

Excess dietary fructose does not alter gut microbiota or permeability in humans: A pilot randomized controlled study - PubMed

In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD.

pubmed.ncbi.nlm.nih.gov

"Results: Routine blood, uric acid, liver function, and lipid measurements were unaffected by the fructose intervention. The fecal microbiome (including Akkermansia muciniphilia), fecal metabolites, gut permeability, indices of endotoxemia, gut damage or inflammation, and plasma metabolites were essentially unchanged by either intervention.
Conclusions: In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD."

Great share!

 

[Hans]

200-300g a day?

Of white sugar? That's likely not a good idea. But if it's from fruit and honey, it shouldn't be an issue.

 

[SamYo123]

Of white sugar? That's likely not a good idea. But if it's from fruit and honey, it shouldn't be an issue.

Right so.. sucrose speeds the metabolism up by 20%, fruit and honey dont do that? Sucrose is honey, and fruit, no?

Also what about Durianrider, who eats 300g+ of sugar and about 5g of fat per day.. no deficiencies?

 

[aniciete]

Right so.. sucrose speeds the metabolism up by 20%, fruit and honey dont do that? Sucrose is honey, and fruit, no?

Also what about Durianrider, who eats 300g+ of sugar and about 5g of fat per day.. no deficiencies?

Who’s to say he doesn’t have deficiencies? Are you him?

 

[Hans]

Right so.. sucrose speeds the metabolism up by 20%, fruit and honey dont do that? Sucrose is honey, and fruit, no?

Also what about Durianrider, who eats 300g+ of sugar and about 5g of fat per day.. no deficiencies?

Why would sucrose speed up the metabolic rate and not fruit?
Does he eat plain white sugar? Perhaps his gut bacteria are creating a ton of B-vitamins.

 

[SamYo123]

Why would sucrose speed up the metabolic rate and not fruit?
Does he eat plain white sugar? Perhaps his gut bacteria are creating a ton of B-vitamins.

View: https://www.youtube.com/watch?v=O5GHBXk2QEM

 

[Jam]

View: https://www.youtube.com/watch?v=O5GHBXk2QEM