Glucose question - Page 2

Go Back   The Diabetes Forum Support Community For Diabetics Online > Diabetes Forum Community > Diabetes Complications

Diabetes Complications Diabetes can cause many short term, long term, acute and chronic complications. Please use this section to discuss any experiences you have with Diabetes related complications. New members please feel free to post about your concerns and ask questions to the community.


Like Tree11Likes

Glucose question - Page 2


Closed Thread
 
Shared Thread Thread Tools
Old 04-27-2012, 20:39   #11
Senior Member
 
Join Date: Dec 2011
Location: Georgia, USA
Posts: 558

Member Type
Type 2
Diagnosed in 2011

530 likes received
240 likes given
Default

Quote:
Originally Posted by smorgan View Post
Or is it possible that the amount of glucose metabolism required for this purpose is so small that it is a non-issue as I was trying to allude to earlier? In ketosis, cells are perfectly capable of metabolising glucose and they do. This is the beauty of this ancestral metabolic state. I call it the "multi-fuel" state. Contrarily, when glucose is constantly supplied, there are no ketones available and FFAs are rarely, if ever, utilized - and it is only some cells which are capable of that in any case. Glucose is a "rude" macro-nutrient and blocks the other two.

So, if you're relying solely on glucose for energy, insulin resistance could mean that cells can't get enough for that purpose. But I suspect the needs you refer to are much smaller and with the pressure off by no longer relying on glucose for ATP, there is a comfortable margin.

Just guessing, but I would suspect that there is no additional redox stress on a ketogenic diet and that the body is smart enough to metabolize sufficient (which, remember, is constantly present and available in the blood) glucose to meet those needs. I find it highly doubtful that there could be such a problem with a ketogenic diet when it is what we evolved for and how we lived for over 99% of our existence. Also, there is no sign or evidence of such things from the millions (2 million in Sweden alone) doing it today.
My post in this thread was a direct response to the initial query about glucose entry into cells and is basic biochemistry fact. My discussion relevant to the relationship between ketogenic diet and redox stress is speculation, and to be honest I don't have many answers. I'm fully aware of the paleo/keto talking points, and even with an incomplete understanding, I am nutritional engaged to the point of always testing positive for ketones. However, a little knowledge can be dangerous, and so I always strive to understand more to better my own personal treatment, but will always refrain from dogmatic statements aiming to suggest a particular therapeutic approach for others.

MCS likes this.
Darbro is offline  
Old 04-28-2012, 11:58   #12
Moderator
 
mbuster's Avatar
 
Join Date: Sep 2011
Location: SW Arkansas
Posts: 9,366

Member Type
Type 2
Diagnosed in Feb. 2012

11312 likes received
6596 likes given
Default

Here's a serious question for y'all. We're Betty Rubble's and Wilma Flintstone's slim features an indicator they were in Ketosis.

__________________
Think I've had this since 2003. Told I was Type 2 lean on 2/13/12.
a1c 8.8 (8/2011) 5.2 (02/2020)
TC 183 LDL 102 HDL 65 TG 52 (02/20/2020)
Supplemental vitamins and electrolytes
65 YY Love the LCHF diet. The cheese goes well with my whine

updated 10/12/2020
mbuster is online now  
Old 04-28-2012, 14:18   #13
Senior Member
 
Join Date: Jul 2011
Location: California, USA
Posts: 3,076

Member Type
Type 2
Diagnosed in 2009

4566 likes received
542 likes given
Default

Quote:
Originally Posted by Darbro View Post
My post in this thread was a direct response to the initial query about glucose entry into cells and is basic biochemistry fact. My discussion relevant to the relationship between ketogenic diet and redox stress is speculation, and to be honest I don't have many answers. I'm fully aware of the paleo/keto talking points, and even with an incomplete understanding, I am nutritional engaged to the point of always testing positive for ketones. However, a little knowledge can be dangerous, and so I always strive to understand more to better my own personal treatment, but will always refrain from dogmatic statements aiming to suggest a particular therapeutic approach for others.
OK, thanks for clearing up that the latter part was purely speculative. And thanks again for causing me to go research lots of new things!

I believe I have found most of what you have proposed to be the opposite of what has actually been found regarding the relationship between KD and ROS and oxidative stress. Here's what I understood you to be saying:

Since glucose metabolism results in NADPH which is critical to the "glutathione antioxidant defense system" and the KD means reduced glucos metabolism, it would be expected to result int:

- reduced glutathione and hence "aberrant redox stress".

- I believe you proposed somewhere in there an increase in the production of ROS in the mitochondria.

1. KD reduces, not increases production of reactive oxygen species

Abstract

Anticonvulsant mechanisms of the ketogenic diet. [Epilepsia. 2007] - PubMed - NCBILink
Quote:
The ketogenic diet (KD) is a broadly effective treatment for medically refractory epilepsy. Despite nearly a century of use, the mechanisms underlying its clinical efficacy remain unknown. In this review, we present one intersecting view of how the KD may exert its anticonvulsant activity against the backdrop of several seemingly disparate mechanistic theories. We summarize key insights gleaned from experimental and clinical studies of the KD, and focus particular attention on the role that ketone bodies, fatty acids, and limited glucose may play in seizure control. Chronic ketosis is anticipated to modify the tricarboxcylic acid cycle to increase GABA synthesis in brain, limit reactive oxygen species (ROS) generation, and boost energy production in brain tissue. Among several direct neuro-inhibitory actions, polyunsaturated fatty acids increased after KD induce the expression of neuronal uncoupling proteins (UCPs), a collective up-regulation of numerous energy metabolism genes, and mitochondrial biogenesis. These effects further limit ROS generation and increase energy production. As a result of limited glucose and enhanced oxidative phosphorylation, reduced glycolytic flux is hypothesized to activate metabolic K(ATP) channels and hyperpolarize neurons and/or glia. Although it is unlikely that a single mechanism, however well substantiated, will explain all of the diet's clinical benefits, these diverse, coordinated changes seem poised to stabilize synaptic function and increase the resistance to seizures throughout the brain.
2. The KD increases, not decreases levels of glutathione.

Link
Quote:
Abstract
The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. We sought to determine whether the KD improves mitochondrial redox status. Adolescent Sprague–Dawley rats (P28) were fed a KD or control diet for 3 weeks and ketosis was confirmed by plasma levels of β-hydroxybutyrate (BHB). KD-fed rats showed a twofold increase in hippocampal mitochondrial GSH and GSH/GSSG ratios compared with control diet-fed rats. To determine whether elevated mitochondrial GSH was associated with increased de novo synthesis, the enzymatic activity of glutamate cysteine ligase (GCL) (the rate-limiting enzyme in GSH biosynthesis) and protein levels of the catalytic (GCLC) and modulatory (GCLM) subunits of GCL were analyzed. Increased GCL activity was observed in KD-fed rats, as well as up-regulated protein levels of GCL subunits. Reduced CoA (CoASH), an indicator of mitochondrial redox status, and lipoic acid, a thiol antioxidant, were also significantly increased in the hippocampus of KD-fed rats compared with controls. As GSH is a major mitochondrial antioxidant that protects mitochondrial DNA (mtDNA) against oxidative damage, we measured mitochondrial H2O2 production and H2O2-induced mtDNA damage. Isolated hippocampal mitochondria from KD-fed rats showed functional consequences consistent with the improvement of mitochondrial redox status i.e. decreased H2O2 production and mtDNA damage. Together, the results demonstrate that the KD up-regulates GSH biosynthesis, enhances mitochondrial antioxidant status, and protects mtDNA from oxidant-induced damage.

__________________
Salim Morgan, T2
66 Years
DX: 9/2009 A1C=10.7
A1C 2/2010: 6.7 (DX + 4 months)
A1C 5/2010: 6.0 (DX + 8 months)
A1C 8/2010: 5.7 (DX + 11 months)
A1C 11/2010: 5.1 (DX + 14 months)
A1C 9/2011: 5.6 (DX + 2 years)
A1C 7/2012: 5.5 (DX + 2 years 10 months)
A1C 1/2019: 5.5
Diet: Approximately C:10;P:15;F:75 (as % calories)
Exercise: Not much. Stairs at home & work.
NO MEDS, No Highs, No Lows
Grandkids: 22
smorgan is offline  
 
Old 04-28-2012, 15:15   #14
Senior Member
 
Join Date: Dec 2011
Location: Georgia, USA
Posts: 558

Member Type
Type 2
Diagnosed in 2011

530 likes received
240 likes given
Default

Glad I've inspired some digging ....and yes, I had seen those and a few related stories closer to my dx when looking at solutions. The antioxidant effect has been suggested to be due to activation of another antioxidant pathway (Nrf2) to compensate. It is complicated and more research is needed, particularly in humans, and more importantly in non-neuronal tissues such as the pancreas. Also important epithelia relevant to cancer, where the media has pushed antioxidants forever and now the story isn't as clear. The key is in the interpretation and action on limited literature. That said, it's better to have the epilepsy papers suggesting a positive relationship between KD and redox stress than otherwise

Darbro is offline  
Old 04-28-2012, 18:57   #15
Senior Member
 
Join Date: Jul 2011
Location: California, USA
Posts: 3,076

Member Type
Type 2
Diagnosed in 2009

4566 likes received
542 likes given
Default I Missed This One

Here's one of the most interesting studies I found about the anti-inflammatory properties of ketogenic diets:

ScienceDirect.com - Neuroscience - Ketones inhibit mitochondrial production of reactive oxygen species production following glutamate excitotoxicity by increasing NADH oxidation

__________________
Salim Morgan, T2
66 Years
DX: 9/2009 A1C=10.7
A1C 2/2010: 6.7 (DX + 4 months)
A1C 5/2010: 6.0 (DX + 8 months)
A1C 8/2010: 5.7 (DX + 11 months)
A1C 11/2010: 5.1 (DX + 14 months)
A1C 9/2011: 5.6 (DX + 2 years)
A1C 7/2012: 5.5 (DX + 2 years 10 months)
A1C 1/2019: 5.5
Diet: Approximately C:10;P:15;F:75 (as % calories)
Exercise: Not much. Stairs at home & work.
NO MEDS, No Highs, No Lows
Grandkids: 22

Last edited by smorgan; 04-28-2012 at 19:00.
smorgan is offline  
Closed Thread

Tags
cellular activation, glucose, insulin

Thread Tools

Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

BB code is On
Smilies are On
[IMG] code is On
HTML code is Off
Trackbacks are On
Pingbacks are On
Refbacks are Off


Similar Threads
Thread Thread Starter Forum Replies Last Post
Question about Insulin vs Glucose levels Peter_V Diabetes 0 10-16-2011 07:33
Glucose tablets question audiogatorjim Diabetes Symptoms 2 03-21-2011 18:10
Technical question about glucose level and energy Libby Diabetes 4 12-15-2010 16:24
question about food effecting blood glucose Joshua Shorter Diabetes 3 07-16-2010 22:57
Normal evening glucose, high fasting glucose Dusper Diabetes 1 11-22-2008 16:13

LEGAL NOTICE
By using this Website, you agree to abide by our Terms and Conditions (the "Terms"). This notice does not replace our Terms, which you must read in full as they contain important information. You must not post any defamatory, unlawful or undesirable content, or any content copied from a third party, on the Website. You must not copy material from the Website except in accordance with the Terms. This Website gives users an opportunity to share information only and is not intended to contain any advice which you should rely upon. It does not replace the need to take professional or other advice. We have no liability to you or any other person in respect of any content on this Website.


All times are GMT +1. The time now is 05:40.




Powered by vBulletin®
Copyright ©2000 - 2020, vBulletin Solutions, Inc.
Search Engine Optimization by vBSEO
vBulletin Security provided by vBSecurity v2.2.2 (Pro) - vBulletin Mods & Addons Copyright © 2020 DragonByte Technologies Ltd.
User Alert System provided by Advanced User Tagging v3.1.0 (Pro) - vBulletin Mods & Addons Copyright © 2020 DragonByte Technologies Ltd.