Excessive consumption of fructose-rich foods has been suggested to contribute to negative health outcomes. [1] [2] [3] Unlike glucose, whose metabolism is more rigorously controlled by the PFK1 enzyme, fructose is regulated and processed through metabolic pathways in a less complex manner. Fructokinase, the enzyme that activates fructose intracellularly via phosphorylation to commence its utilization, is not subject to negative feedback control from the downstream intermediates of glycolysis, the TCA cycle, or energy carriers. [4] [5] [6] This can result in large amounts of acetyl-CoA originating from the metabolism of fructose being fed into fatty acid biosynthesis pathways. [7] [8] This increased flux through the fatty acid pathways results in highly elevated generation and accumulation rates for various fats. In some hibernating mammals, it is suggested that this deregulated utilization of fructose might have an advantageous adaptive role. [9] Rapid generation of fat storage when animals feed before the winter on seasonal ripe fruits, which are high in fructose, allows them to build a significant energy storage in a short time period. In some animals that are native to locations with pronounced seasonality, this mechanism also can contribute to fat accumulation to increase robustness and survive resource-scarce winters. [10] It is argued that this mechanism is also present in primates, including humans. Furthermore, its residual effects may cause more harm than benefit as hibernation is not a selective pressure in modern society and human metabolism has not evolved to handle excessive caloric/carbohydrate intake. [5] [10]
Moderate fruit consumption does not usually increase the blood levels of fructose since the small intestine uses it to generate glucose. [11] However, when fructose is artificially added in foods or when excessive amounts of fructose or sucrose-rich fruit is consumed, it can noticeably reach the systemic circulation. [12] The systemic bioavailability of fructose is positively correlated with increased de novo lipogenesis, decreased fatty acid oxidation, increased liver fat, postprandial triglycerides, cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL)-C, and C-reactive protein. These effects are substantially more pronounced in regards to fructose consumption when compared to excessive glucose intake. [13] Moreover, the lipogenic effects of fructose are exacerbated with the associated uptake of saturated fatty acids. [14] This compounding effect is quite likely fueled by diets containing fast foods that are both highly sweetened and processed in oils or high in fat. [15]
Fructose metabolism intermediates can also activate the glycolytic pathway by entering through glyceraldehyde-3-phosphate and dihydroxyacetone phosphate, which could be especially detrimental in cancer due to the Warburg effect. [16] Transient intracellular phosphate depletion due to the excessive phosphorylation of fructose by fructokinase may also affect purine metabolism resulting in increased production of uric acid. Uric acid, in turn, may further promote lipogenesis, as well as mediate other pathological processes that play an important role in the development of metabolic syndrome, high blood pressure, and gout. [17] Negative metabolic effects of fructose are compounded by its inability, unlike glucose, to induce satiety. This may be the reason for less controlled or excessive consumption of fructose-rich foods. [18]
Hereditary fructokinase deficiency does not appear to have any apparent negative health effects in humans [19] and may actually be associated with a better prognosis in populations where diets include large amounts of fructose. [20] It is possible that without normal fructokinase activity, metabolism of exogenous fructose would be decreased since fructose metabolites would be able to neither feed in acetyl-CoA generation nor upregulate lipid synthesis and accumulation. The excessive amount of fructose will simply be excreted with urine resulting in fructosuria, which is virtually a harmless health condition that could be incidentally found during a medical check-up for unrelated reasons. [21] It is shown that fructokinase inhibition might also be beneficial in ischemic acute kidney injury since, under this condition, fructose mediates oxidative stress and cell injury. [22] [23] It is suggested that preventing or decreasing the metabolism of exogenous fructose will be beneficial in terms of carbohydrate and lipid metabolism as well as will decrease uric acid production which is beneficial as increased uric acid buildup triggers oxidative stress and inflammation. [24] Luteolin, an ingredient in some dietary supplements, was used in animal studies to inhibit fructose metabolism and showed beneficial effects in disrupting pathological processes mediated by fructose. However, the clinical relevance of these findings for humans is not known. [25]
Hello, I'm
Zefr. I noticed that you added or changed content in an article,
Fructose, but you didn't provide a
reliable source. It's been removed and archived in the page history for now, but if you'd like to
include a citation and re-add it, please do so. You can have a look at the
tutorial on citing sources. If you think I made a mistake, you can leave me a message on
my talk page. Introduce major changes and controversial topics first on the talk page, then engage in discussion to obtain
WP:CON.
Zefr (
talk)
15:13, 2 March 2021 (UTC)
References
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
It's evident from this draft that you are writing a term paper (NOTESSAY, NOTJOURNAL) rather than synthesizing established facts based on review articles. All your sources are primary research, not MEDRS reviews, and your text is a narrative of speculation (fine for a thesis or journal report) rather than review-established facts. Your text includes terms like "likely", "could be", "may also", "suggested", etc. which are not encyclopedic terms and facts. I suggest you spend some time absorbing MEDRS, MEDHOW, and WHYMEDRS to understand better the need for conclusive review sources, then write concise statements supported by high-quality reviews. Zefr ( talk) 16:52, 2 March 2021 (UTC)
![]() |
Hello, Pippin2k!
Having an article declined at Articles for Creation can be disappointing. If you are wondering why your article submission was declined, please post a question at the
Articles for creation help desk. If you have any other questions about your editing experience, we'd love to help you at the
Teahouse, a friendly space on Wikipedia where experienced editors lend a hand to help new editors like yourself! See you there!
DoubleGrazing (
talk)
13:13, 30 April 2022 (UTC)
|
An article you recently created,
Bernhard Landwehrmeyer, is not suitable as written to remain published. It needs more citations from
reliable,
independent sources. (
?) Information that can't be referenced should be removed (
verifiability is of
central importance on Wikipedia). I've moved your draft to
draftspace (with a prefix of "Draft:
" before the article title) where you can incubate the article with minimal disruption. When you feel the article meets Wikipedia's
general notability guideline and thus is ready for mainspace, please click on the "Submit your draft for review!" button at the top of the page.
DoubleGrazing (
talk)
13:21, 30 April 2022 (UTC)
Your edit to
Draft:Bernhard Landwehrmeyer has been removed in whole or in part, as it appears to have added
copyrighted material to Wikipedia without evidence of
permission from the copyright holder. If you are the copyright holder, please read
Wikipedia:Donating copyrighted materials for more information on uploading your material to Wikipedia. For legal reasons, Wikipedia cannot accept copyrighted material, including text or images from print publications or from other websites, without an appropriate and verifiable license. All such contributions will be deleted. You may use external websites or publications as a source of information, but not as a source of content, such as sentences or images—you must write using your own words. Wikipedia takes copyright very seriously, and persistent violators of our copyright policy will be
blocked from editing. See
Wikipedia:Copying text from other sources for more information. —
Diannaa (
talk)
13:48, 2 May 2022 (UTC)
Your message on my talk page:
Hello DoubleGrazing! I've amended the draft and added many sources, mainly from scientific journals where Prof. Landwehrmeyer is a author or contributor. I kindly ask you to review this article since it is important for him in his career advancement, which will benefit many patients with Huntington's disease, a rare, severe, debilitating disorder. — Preceding unsigned comment added by Pippin2k ( talk • contribs) 14:20, 2 May 2022 (UTC) DoubleGrazing ( talk) 14:35, 2 May 2022 (UTC)
Hello, Pippin2k. We
welcome your contributions, but if you have an external relationship with the people, places or things
you have written about on the page
Draft:Bernhard Landwehrmeyer, you may have a
conflict of interest (COI). Editors with a conflict of interest may be unduly influenced by their connection to the topic. See the
conflict of interest guideline and
FAQ for organizations for more information. We ask that you:
In addition, you are required by the Wikimedia Foundation's terms of use to disclose your employer, client, and affiliation with respect to any contribution which forms all or part of work for which you receive, or expect to receive, compensation. See Wikipedia:Paid-contribution disclosure.
Also, editing for the purpose of advertising, publicising, or promoting anyone or anything is not permitted. Thank you. DoubleGrazing ( talk) 14:57, 2 May 2022 (UTC)
Congratulations, and thank you for helping expand the scope of Wikipedia! We hope you will continue making quality contributions.
The article has been assessed as C-Class, which is recorded on its talk page. This is a great rating for a new article, and places it among the top 20% of accepted submissions — kudos to you! You may like to take a look at the grading scheme to see how you can improve the article.
If you have any questions, you are welcome to ask at the help desk. Once you have made at least 10 edits and had an account for at least four days, you will have the option to create articles yourself without posting a request to Articles for creation.
If you would like to help us improve this process, please consider
.Thanks again, and happy editing!
Somej ( talk) 21:05, 5 August 2022 (UTC)Hello, Pippin2k. Thank you for creating Bernhard Landwehrmeyer. User:Scope creep, while examining this page as a part of our page curation process, had the following comments:
Great article!!
To reply, leave a comment here and begin it with {{Re|Scope creep}}
. Please remember to sign your reply with ~~~~
. (Message delivered via the
Page Curation tool, on behalf of the reviewer.)
scope_creep Talk 15:12, 7 September 2022 (UTC)
Excessive consumption of fructose-rich foods has been suggested to contribute to negative health outcomes. [1] [2] [3] Unlike glucose, whose metabolism is more rigorously controlled by the PFK1 enzyme, fructose is regulated and processed through metabolic pathways in a less complex manner. Fructokinase, the enzyme that activates fructose intracellularly via phosphorylation to commence its utilization, is not subject to negative feedback control from the downstream intermediates of glycolysis, the TCA cycle, or energy carriers. [4] [5] [6] This can result in large amounts of acetyl-CoA originating from the metabolism of fructose being fed into fatty acid biosynthesis pathways. [7] [8] This increased flux through the fatty acid pathways results in highly elevated generation and accumulation rates for various fats. In some hibernating mammals, it is suggested that this deregulated utilization of fructose might have an advantageous adaptive role. [9] Rapid generation of fat storage when animals feed before the winter on seasonal ripe fruits, which are high in fructose, allows them to build a significant energy storage in a short time period. In some animals that are native to locations with pronounced seasonality, this mechanism also can contribute to fat accumulation to increase robustness and survive resource-scarce winters. [10] It is argued that this mechanism is also present in primates, including humans. Furthermore, its residual effects may cause more harm than benefit as hibernation is not a selective pressure in modern society and human metabolism has not evolved to handle excessive caloric/carbohydrate intake. [5] [10]
Moderate fruit consumption does not usually increase the blood levels of fructose since the small intestine uses it to generate glucose. [11] However, when fructose is artificially added in foods or when excessive amounts of fructose or sucrose-rich fruit is consumed, it can noticeably reach the systemic circulation. [12] The systemic bioavailability of fructose is positively correlated with increased de novo lipogenesis, decreased fatty acid oxidation, increased liver fat, postprandial triglycerides, cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL)-C, and C-reactive protein. These effects are substantially more pronounced in regards to fructose consumption when compared to excessive glucose intake. [13] Moreover, the lipogenic effects of fructose are exacerbated with the associated uptake of saturated fatty acids. [14] This compounding effect is quite likely fueled by diets containing fast foods that are both highly sweetened and processed in oils or high in fat. [15]
Fructose metabolism intermediates can also activate the glycolytic pathway by entering through glyceraldehyde-3-phosphate and dihydroxyacetone phosphate, which could be especially detrimental in cancer due to the Warburg effect. [16] Transient intracellular phosphate depletion due to the excessive phosphorylation of fructose by fructokinase may also affect purine metabolism resulting in increased production of uric acid. Uric acid, in turn, may further promote lipogenesis, as well as mediate other pathological processes that play an important role in the development of metabolic syndrome, high blood pressure, and gout. [17] Negative metabolic effects of fructose are compounded by its inability, unlike glucose, to induce satiety. This may be the reason for less controlled or excessive consumption of fructose-rich foods. [18]
Hereditary fructokinase deficiency does not appear to have any apparent negative health effects in humans [19] and may actually be associated with a better prognosis in populations where diets include large amounts of fructose. [20] It is possible that without normal fructokinase activity, metabolism of exogenous fructose would be decreased since fructose metabolites would be able to neither feed in acetyl-CoA generation nor upregulate lipid synthesis and accumulation. The excessive amount of fructose will simply be excreted with urine resulting in fructosuria, which is virtually a harmless health condition that could be incidentally found during a medical check-up for unrelated reasons. [21] It is shown that fructokinase inhibition might also be beneficial in ischemic acute kidney injury since, under this condition, fructose mediates oxidative stress and cell injury. [22] [23] It is suggested that preventing or decreasing the metabolism of exogenous fructose will be beneficial in terms of carbohydrate and lipid metabolism as well as will decrease uric acid production which is beneficial as increased uric acid buildup triggers oxidative stress and inflammation. [24] Luteolin, an ingredient in some dietary supplements, was used in animal studies to inhibit fructose metabolism and showed beneficial effects in disrupting pathological processes mediated by fructose. However, the clinical relevance of these findings for humans is not known. [25]
Hello, I'm
Zefr. I noticed that you added or changed content in an article,
Fructose, but you didn't provide a
reliable source. It's been removed and archived in the page history for now, but if you'd like to
include a citation and re-add it, please do so. You can have a look at the
tutorial on citing sources. If you think I made a mistake, you can leave me a message on
my talk page. Introduce major changes and controversial topics first on the talk page, then engage in discussion to obtain
WP:CON.
Zefr (
talk)
15:13, 2 March 2021 (UTC)
References
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
It's evident from this draft that you are writing a term paper (NOTESSAY, NOTJOURNAL) rather than synthesizing established facts based on review articles. All your sources are primary research, not MEDRS reviews, and your text is a narrative of speculation (fine for a thesis or journal report) rather than review-established facts. Your text includes terms like "likely", "could be", "may also", "suggested", etc. which are not encyclopedic terms and facts. I suggest you spend some time absorbing MEDRS, MEDHOW, and WHYMEDRS to understand better the need for conclusive review sources, then write concise statements supported by high-quality reviews. Zefr ( talk) 16:52, 2 March 2021 (UTC)
![]() |
Hello, Pippin2k!
Having an article declined at Articles for Creation can be disappointing. If you are wondering why your article submission was declined, please post a question at the
Articles for creation help desk. If you have any other questions about your editing experience, we'd love to help you at the
Teahouse, a friendly space on Wikipedia where experienced editors lend a hand to help new editors like yourself! See you there!
DoubleGrazing (
talk)
13:13, 30 April 2022 (UTC)
|
An article you recently created,
Bernhard Landwehrmeyer, is not suitable as written to remain published. It needs more citations from
reliable,
independent sources. (
?) Information that can't be referenced should be removed (
verifiability is of
central importance on Wikipedia). I've moved your draft to
draftspace (with a prefix of "Draft:
" before the article title) where you can incubate the article with minimal disruption. When you feel the article meets Wikipedia's
general notability guideline and thus is ready for mainspace, please click on the "Submit your draft for review!" button at the top of the page.
DoubleGrazing (
talk)
13:21, 30 April 2022 (UTC)
Your edit to
Draft:Bernhard Landwehrmeyer has been removed in whole or in part, as it appears to have added
copyrighted material to Wikipedia without evidence of
permission from the copyright holder. If you are the copyright holder, please read
Wikipedia:Donating copyrighted materials for more information on uploading your material to Wikipedia. For legal reasons, Wikipedia cannot accept copyrighted material, including text or images from print publications or from other websites, without an appropriate and verifiable license. All such contributions will be deleted. You may use external websites or publications as a source of information, but not as a source of content, such as sentences or images—you must write using your own words. Wikipedia takes copyright very seriously, and persistent violators of our copyright policy will be
blocked from editing. See
Wikipedia:Copying text from other sources for more information. —
Diannaa (
talk)
13:48, 2 May 2022 (UTC)
Your message on my talk page:
Hello DoubleGrazing! I've amended the draft and added many sources, mainly from scientific journals where Prof. Landwehrmeyer is a author or contributor. I kindly ask you to review this article since it is important for him in his career advancement, which will benefit many patients with Huntington's disease, a rare, severe, debilitating disorder. — Preceding unsigned comment added by Pippin2k ( talk • contribs) 14:20, 2 May 2022 (UTC) DoubleGrazing ( talk) 14:35, 2 May 2022 (UTC)
Hello, Pippin2k. We
welcome your contributions, but if you have an external relationship with the people, places or things
you have written about on the page
Draft:Bernhard Landwehrmeyer, you may have a
conflict of interest (COI). Editors with a conflict of interest may be unduly influenced by their connection to the topic. See the
conflict of interest guideline and
FAQ for organizations for more information. We ask that you:
In addition, you are required by the Wikimedia Foundation's terms of use to disclose your employer, client, and affiliation with respect to any contribution which forms all or part of work for which you receive, or expect to receive, compensation. See Wikipedia:Paid-contribution disclosure.
Also, editing for the purpose of advertising, publicising, or promoting anyone or anything is not permitted. Thank you. DoubleGrazing ( talk) 14:57, 2 May 2022 (UTC)
Congratulations, and thank you for helping expand the scope of Wikipedia! We hope you will continue making quality contributions.
The article has been assessed as C-Class, which is recorded on its talk page. This is a great rating for a new article, and places it among the top 20% of accepted submissions — kudos to you! You may like to take a look at the grading scheme to see how you can improve the article.
If you have any questions, you are welcome to ask at the help desk. Once you have made at least 10 edits and had an account for at least four days, you will have the option to create articles yourself without posting a request to Articles for creation.
If you would like to help us improve this process, please consider
.Thanks again, and happy editing!
Somej ( talk) 21:05, 5 August 2022 (UTC)Hello, Pippin2k. Thank you for creating Bernhard Landwehrmeyer. User:Scope creep, while examining this page as a part of our page curation process, had the following comments:
Great article!!
To reply, leave a comment here and begin it with {{Re|Scope creep}}
. Please remember to sign your reply with ~~~~
. (Message delivered via the
Page Curation tool, on behalf of the reviewer.)
scope_creep Talk 15:12, 7 September 2022 (UTC)