Metformin - Science topic

I did an experiment for a positive control phos-tag system to detect phosphorylated AMPK in min6 cells. I incubated min6 cells for 12h with metformin to induce AMPK phosphorylation then check the result by phospho-specific antibody and get a confirmation of increased phosphorylation but after I check with phostag system I did not get the result that I expected. Anyone has experience in this technique, your feed back is appreciated. here I include my result and condition

CAN ANYONE PLEASE HELP ME WITH THIS QUESTION?

I HAVE READ MANY MANY ARTICLES ABOUT THE POSITIVE CORRELATION BETWEEN THE TWO VARIABLES BUT NO ONE DESCRIBED AN UNDERLYING MECHANISM.

PLEASE SHED SOMETIME

"'Metformin improves insulin sensitivity, promotes cellular repair, is anti-inflammatory, and antioxidant. All these properties contribute to its anti-aging effects,' Merrill told us. Studies in people with type 2 diabetes have shown that metformin activates the AMP-activated protein kinase (AMPK).

7 may 2024 "( https://www.medicalnewstoday.com/articles/why-do-some-researchers-believe-metformin-may-hold-the-key-to-longevity ).

Can you explain the off-label uses of metformin discussed in the review?

What are the primary indications for metformin usage according to the FDA?

Why does the ADA recommend metformin for individuals with prediabetes?

What are some potential contraindications to metformin therapy?

How does metformin compare to other antidiabetic medications in terms of efficacy and safety?

What ongoing research is being conducted to explore metformin's potential in antiaging, anticancer, and neuroprotective effects?

How important is patient education in ensuring optimal outcomes with metformin therapy?

What role does the interprofessional healthcare team play in managing patients on metformin?

Can you discuss some common adverse effects associated with metformin use?

How might the future of metformin therapy evolve based on current research trends and advancements in diabetes care?

Are there any published papers on the comparison between the effect of metformin and oral cotraceptive pills on polycystic overian syndrome?

I'm working on cancer biology in AMPK pathway.

I use some AMPK activator like metformin, and when I treat that activator, I detect the phospho-AMPK (Thr172) is increasing in western blot data.

And I treat the Compound C in same sample, but the phospho-AMPK is extremely upregulated!

I saw same result in many times. I don't know how to troubleshoot.

I never saw in any paper that using Compound C. All of the references show phospho-AMPK is decreased when Compound C treat.

I already try pretreatment method, and ATP adding method.

Is there anything that can I do??

If someone use the Compound C, please tell me detail procedure..

Hello,

We need the pdb of metformin for docking studies in ClusPro.

We tried to make it from the 5G5J pdb but that pdb does not work in ClusPro. I added the pdb we made by splitting from 5G5J. Pymol can recognize it but not ClusPro.

Any recommendation would be helpful.

Thanks,

Bidisha

Anemia with low normal MCV, ferritin, serum iron refractory to iron and folate supplements. Other causes of anemia have been ruled out like GI pathology. Other cell lines WBC and differential and platelets are normal. These side effects have been described in the literature. Metformin can cause B12 deficiency and macrocytic anemia due to reduced absorption in the GI tract. ACEI can rarely cause anemia due to concurrent inhibition of erythropoietin and RBC synthesis. Has anyone seen these effects in clinical practice?

I work with cultured cells which I treat with metformin prepared in aqueous solution. I keep the stock at 4°C but I have noticed that after a few months it stops doing what it usually does in my biological system. I would like to know if anyone knows the approximate half-life in aqueous solution. Thank you

I am facing an issue with the dissolution profile of Sitagliptin and metformin tablets ,there is significant drop in dissolution release of both components while compared with initial dissolution profile..

Salam (Greetings),

I'm working on Metformin and wanna test its effect on some cell lines when combined with other drugs, which are mainly soluble in DMSO.

I've looked up metformin solubility and found it soluble in both water (up to 2 M) and, to less extent, in DMSO (up to 100 mM).

My question is: which one should I use to prepare it?

- Both stock and serial dilutions with DMSO, while maintaining its concentration <0.5%

- Stock with DMSO and serial dilution with water

- Both stock and serial dilutions with water

I would appreciate sharing ur experience and enlightening me with the pros and cons, if any.

Thank you

im clinical pharmacist , i would like to ask why sometimes endocrinologist prefer initiating Pioglitazone with metformin for managing diabetes type 2 patients meanwhile, there are much better treatment option are available managing type 2 diabetes ?

Regards

How Metformin and exercise affects the plasma glucose concentration?

I was reviewing data glycted haemoglobin in patients with type-2 diabetes. Some patients seem to respond excellent metformin but some just do not did well. Yes i confirmed associated life style changes and some times their dosages were increased by concerned physicians.

Reviewing the data showed the some polymorphism affecting he metformin response. These were few that eent through my literature search: SLC22A2 rs316019 and SLC47A2 rs12943590 and were probably associated with good response in comparison to patients who carry the G‐allele type.

Because we are so blind-folded in prescribing metformin as a starter to every type -2 diabetics, i was wondering how significant these genetic polymorphysims/mutations are in reality? Should they not matter in a patient who has to take metformin for life????

Can anybody elaborate on this?

Regards

I need to write a critical analysis of this paper ( ) and I have a question regarding dropout rates. 25% of the participants in the trial decrease the dose of the drug they are taking due to side effects. Would these participants be considered dropouts?

The authors perform statistical analyses including and excluding these participants. Would excluding these participants dramatically reduce the power of the analysis?

Thank you,

a confused student.

We are performing an antidiabetic assay by inducing alloxan in rats and we have to share with metformin, glibenclamide, or actrapid for the positive control.

Which of these three drugs is the best to use?

For undergraduate lab class

We would like to treat our tissue culture cells with metformin, so the metformin needs to be sterile, TC specific. Any local distributors or is it ok to just sterile filter?

I am having an issue regarding sitagliptin 50mg and Metformin 1000 mg formulation (Janumet formula)… Tablets are very weak and Friability 0.6% hardness NMT 25 Kp… Which causes splitting, capping and broken edges during coating process.

Is there any chance to solve this issue??

I am working on MDA-MB-231cell line and kind of a modified drug, metformin that we made in our labratory for better intestinal premeation.both metformin and modified metformin had a good effect on deacreasing invasion but surprisingly did not prevent its migration.how its possible ?

Is there a reason why the pioneering and potentially important findings of Dr. Gualano (Gualano B, Creatine in type 2 diabetes: a randomized, double-blind, placebo-controlled trial. Med Sci Sports Exerc. 2011May;43(5) showing! ~1% decrease of HBa1c in patients taking creatine supplements even in the presence of metformin !) were not tested anywhere in larger clinical trials?

Hello everyone. I am curently working on a protocol to measure glucose uptake in HepG2 cells using 2-NDBG. The work involves the pre-treatment of cells with an active material and observe if it has an effect on increasing glucose uptake. Metformin is used as a positive control. I have come across several threads on ReaserchGate which gave me the impression that this experiment is kind of tricky.

I have read several references. In some references, the cells are pre-treated with the drug, next incubated with glucose-free medium, and lastly the fluorescent 2-NBDG (in glucose-free medium) is added. In others, after incubation with the drug and before the addition of 2-NBDG, there is an extra step in which cells are stimulated with insulin for only 15 min.

I have a couple of questions.

Lately, there have been wave upon wave of recalled medicine since FDA has been starting doing an investigation on present of problematic human carcinogen substance which is NDMA in mostly common prescribed drug such as Ranitidine. The latest news has mentioned that Glucophage (Metformin) has been suspected to have NDMA as well. Why do you think that this finding was not discovered before, and we have only recently started to hear about this critical threat that exists in mostly used medications?. Is it because pharmaceutical companies have started to not follow strictly Good Manufacturing Practice (GMP) ?

let me know the complete reaction for electrooxidation/electrocoagulation mineralization of metformin in water environment? whether ammonium ion will form or nitrate ion will form.

Metformin, not only an extensively used oral hypoglycemic agent, but also a proven antimalarial and antiviral. I request that someone analyze the two groups treated for COVID-19, comparing those already on metformin, versus not. Thank you.

In the case of controversial outcome, was chloroquine administered to COVID-19 patients in combination with drugs inducing an acid environment (i.e. beta blockers, statins, metformin, some antibiotics etc.)? Should it be the case, these drugs might hinder or compensate the beneficial effect of chloroquine. It would be interesting in testing its effectiveness alone or in combination with a drug/substance inducing an alkaline environment.

The most difficult scientific advances become possible when you ask the right question. In the case of COVID-19, I understand that the right question is: why do some people become seriously infected when exposed to low viral load, while others are not sick even when exposed to high viral loads? The situation resembles the film The Andromeda Strain, which I used for many years as an example of scientific research in my Philosophy of Science classes. There is a deathly virus that came in a spaceship, which kills the vast majority of people. However, a baby and a drunk are immune to the action of this virus. A scientist then asks the right question: why are these two people immune? When investigating the physiology of these people, he discovers that both have their PH in certain ranges, the baby alkaline due to excessive crying, and the drunk acid from the ingested drink. In the case of Corona, we have indicators that its action occurs mainly in the mitochondria (see Castalia Francon´s insights below), which has an evolutionary origin due to endosymbiosis (when the eukaryotic cell incorporates bacteria that help it perform certain functions). Mitochondrial DNA is exclusively maternal in origin. Some factors that affect the mitochondria, such as nicotine and metformin, may predispose to the action of the virus. All this indicates that it is necessary to research the affinity of the virus with certain segments of the mitochondrial DNA, to verify if there is a segment present in the mitochondrial DNA of susceptible people, which is not found in the DNA of people not susceptible to the disease. After this discovery CRISPR technology may be used succssfully.

The mechanisms of action of Metformin against Diabetes, boosting mitochondria and reducing the stress caused by excess glucose, may be useful for the fight against the new Coronavirus. I have discussed with experts the action of Metformin and its relation to cancer tumor genesis in another RG question (https://www.researchgate.net/post/Does_the_use_of_metformin_against_type_2_diabetes_increase_or_decrease_the_probability_of_appearance_of_cancer_tumors).

To answer the above question, it is necessary to take into account recent data on the mechanism of action of the virus and empirical statistical (positive or negative) correlation between use of Metformin and the lethality of the virus. Is there any data on this correlation?

According to comments by Castalia Francon, "Neutrophils are known as the core of the 'innate immune systems". They are our 'first responders" to any imminent medical holocaust...NETS, 'Neutrophilic Extracellular Traps" as the battlefield. These powerful products of our neutrophils are essentially a nuclear option against the pathogens. As such they do whatever they can to prevent that explosive death of the neutrophil that will ensnare them...

For bacteria and viruses, their goal of survival entails first avoiding, by whatever means they have, the phagocytosis efforts and then countering the next move of the neutrophils, their death by NETosis.

To attempt this, they seek to manipulate the communications between mitochondria and the cell so as to stall the Neutrophil in a limbo known as "autophagy" while the microbe can continue to reproduce and spread.

The term "autophagy" came into use to denote a systematic, almost "thoughtful" process by means of which the neutrophils, just like macrophages, could move sequentially through a series of considerations pertaining to how to deal with their situation in terms of life and death. But by its very nature as an extremely complex process entailing many dimensional considerations, it is also readily exploitable by pathogens, and in particular by viruses

Many pathogens have been shown to evade or exploit autophagy in macrophages, aiming to establish an intracellular niche for long-term survival and replication Subversion of autophagy by microbes in neutrophils is far less studied but the Corona situation seems to point to it...Our best analogy to it is how when we with to delete", 'our computers ask us, "Are you sure'?" It appears most likely that autophagy is the manifestation of a process that almost always goes on, and eventuates in some adaptive response....unless, of course, the communications between mitochondria and cell are distorted or diminished by pathogen actions.

Viruses and bacteria have evolved over millions of years as each others nemeses, long before we were on the scene, thus the virus is naturally inclined to maniupulate the mitochrondira and by means of that to in turn manipulate the entire cell which is driven by the mitochondria and their needs...

Unfortunately the current 'expert' narrative speaks dichotomously of either "promoting" or 'inhibiting" autophagy instead of coming to terms that there is an ongoing and complex battle going on where any one aspect can shift the nature of the complex decision making.one way or the other. The pathogen, however, is most happy when no clear decisions at all is reached.

The essential treatment for Corona Virus infection is to assure that once the phagocytosis fails....which it often does...that the neutrophils are not stalled from their productive and special death with its Neutrophilic Extracellular Trap creation...which releases the remarkable power of their own DNA to act as a potent immune system weapon against microbes.

We would not be surprised if the CRISPR technology which is now surfacing with so much promise is not an aspect of the manner in which DNA/chromatin sections can be used productively to kill viruses...as they have been used for millennia, apparently, by bacteria.

In summary

• Previous smoking habit is highly associated with the dire effects of Corona Infection....and it also leads to a maladaptive tendency towards' "autophagy" which renders those persons' neutrophils unable to engage in "NETosis " and create "NETS""t

• Smokers neutrophils seem to have phenotypically altered over the course of their previous smoking habit so that they are unable to properly engage in their intense first line of defense, phagocytosis (via NADPH mechanisms).

We only need to observe that in Italy, where the death rates from Corona are soaring, they differ in the terms of their 'lockdown" from ours. Whereas, in the US, pharmacies and groceries and other vital retailers are excluded, in Italy, stunningly, tobacconists and vapes shops join pharmacies as essential and are exempted from lockdown.

Normally, the generation of the ROS products via phagocytosis is a prerequisite for the subsequent death via NETosis.. This is unsurprising since that a failure to be able to engage in phagocytosis would already connote some abnormality or deficit.

•It has however been found that even when the initial phagocytosis does not occur, that, if system can be induced downstream to generate ROS, then NETosis and the creation of those 'traps' is still possible.

• Chloroquine is known to be an "autophagy preventer" in that it can serve to rescue the neutrophil system and thus precipitate the creation of 'NETS. It seems to achieve a mobilization of the NET trap system even though phagocytosis has not succeeded. Exactly what it does is still not clear.

It appears that it is optimal to administer chloroquine early, but only after the first phagocytosis efforts of the neutrophil system but before the virus has seized the opportunity, by manipulating the communications between mitochondria and the cell, to spread and do maximum damage".

I have prepared 500 and 1000 mg metformin tablets with sitagliptin 50 mg respectively. The surface of the tablets although shiny are not smooth and the surface has small blisters. I have checked the tooling and it is fine further when i compress other formulation on the same tooling the tablet surface are smooth. I assume that there is some problem in granulation. we have passed the wet mass through 4 mm mesh and the dried mass through 1.5 mm mesh in an oscillating granulator. Please provide some suggestions to solve the problem.

what is the proper time for administration of metformin in type 2 diabetes ?

Does XR/SR drug affect fasted state? If it was taken prior to fasting, then does the body not enter fasted state until the drug is fully released after 4-8 hours of release?

Hi, I am having trouble getting any elevation in AMPK (PRKAA1) gene expression in k562 cells when I am treating them with Metformin.

Culture system - K562 cells grown in media containing RPMI + 10% Hyclone FBS (Cat no. SH30910.03)

Metformin (Cat no. - 1115-70-4 , Santa Cruz)

I analyzed the gene expression using qPCR and found no elevation in AMPK gene expression when compared with control cells. Kindly let me know what factors I should look into that might be causing this in K562 cells. Thank you

metformin a drug that used to reduce the insulin in peripheral blood of patients with PCOS and then reduce of endrogen ; how the metformin reduce the INS gene expression ??

I have a 60 y.o WF 5 years post total pancreatectomy secondary to cancer. Worsening hypoglycemia with minimal insulin. A1C 9.9%. Any recommendations? Metformin?

After exposing rats to low fructose water(10%) for 2 wks and a single intraperitoneal injection of STZ (55mg/kg bw), to induce T2D, I want to compare the hypoglycaemic effect of my crude plant extract with a known standard drug.

How long will take to adjust the dose of metformin after stable dose therapy is ineffective？ 3 months？

Hi everybody!

I'm performing qRT-PCR for BCR and ABL transcripts from RNA samples. In one patient, the ABL copies are low and we´ve tried everything but we can´t improve it. We then found out that, in this particular case, the patient is taking metformin and fenofibric acid daily, so does anybody know if they could inhibit de PCR?

Thanks!!

Hi,

I am looking for A(1%,1cm) UV-VIS Spectrophotometer reference data for commonly used medicines - such as Metformin, Aspirin and other common medicines. Is there a reference table that is available?

Secondly, does the A(1%,1cm) vary depoending on the solvent used? - for some medicines I see some use Water and some use ethanol?

Dear all, in vitro metformin can nicely lower glucose levels and increase lactate levels which correlates with increased glycolysis. I want to show this in vivo in WT mice, but an IP injection of 100mg/kg could not show hypoglycemia and hyperlactatemia. Anyone suggestions to show increased glycolysis with metformin? Kind regards

What does metformin do to AKT, pGSK3-Beta and Glycogen synthase under insulin signaling ?

Can Metformin use as a medicine for breast cancer?

What are the advantages and disadvantages of using Metformin in patients with breast cancer?

Is it possible to use Metformin for both diabetes mellitus and breast cancer?

Biological Ageing is natural decline and deleterious effects in health and diminishing life span with more diseases like degenerative like Alzhemier, Parkinson in old age, diabetes, cardiovacular diseaes and cancer. Before, 1950s there was no mention of ageing but now its emerging field in research and thinking for better cure of diseases and reverse or delay aging, metformin, rapamycin some antioxidants, herbs and aspirin are screened for anti-aging agents, some trials are needing to finalize the ageing treatments, Hope, in future, there will be less diseases and less early deaths as happening now,

Autoantigen can be used to modulate the immune system and in best case to get tolerance. What/which autoantigen/s? Combinations? Should we combine with antiCD3 and/or TNFalfa-inhibition and/or ? If so, given before , after, or parallell to the auto-antigen treatment? Please argue! Would YOU suggest addition of Vitamin D? Nicotinamide? Omega3 fatty acids? Metformin? or..? We need an open discussion to get forward!

I have a patient who was dx originally in 2012 with stage 3 ovarian cancer. She had complete debulking except for a 1.5 cm tumor implant on the diaphragm and under went 6 cycles of IV chemotherapy resulting in complete remission until October of 2014. At that time the PET showed a possible small tumor implant on the right kidney. Subsequent laparoscopy showed only suspicious washings and she had 6 cycles of IP and IV chemo finishing in 5/15.

In Feb 2018 her PET and CT scans showed retroperitoneal pelvic lymph node recurrence (5 on left, and 3 on the right) and a 2.5 cm liver implant. She was asymptomatic and this was done because of rising CA 125. While she was getting a second opinion for treatment she started herself on a very low carb diet, and I started her on metformin because of she does have prediabetes after reading the positive retrospective studies. The dose was gradually increased to 1500 mg daily.

The lesion on her liver shrunk by 50% by the end of March, and on her last PET scan done 6/15, has disappeared. only 1/5 lymph nodes remain in the left pelvis and the 2 of the 3 lymph nodes on the right side have remained unchanged, with one getting larger. Her CA 125 has decreased by 50% from it's highest level (in March) as of last week.

She would like to continue this treatment. Does anyone have any experience with using metformin for ovarian cancer? She has been measuring her serum ketones but since losing weight finds that she rarely exceeds 0.4. (Weight 118/ height 5'4"). I am suspicious that this is because she does not have that much fat left and apparently metformin decreases free fatty acids. I am also inclined to think the metformin is the key reason for the improvement rather than being in low ketosis.

Any suggestions or thoughts would be appreciated.

I always get less quantity of API than it should be. Often the difference is not more than 50 mg per tablet for both 750 or 1000 mg doses. The EP methodology doesn't work. Please, help me to figure it out

I have compressed tablets of granulates made by continuous twin screw granulation. I have done this for the three following formulations:

- mebendazole 5% + 5% HPMC + 90%lactose

- metformin 5% + 5% HPMC + 90%lactose

- metformin 5% + 5% HPMC + 45%MCC + 45%lactose

Now I was wondering which tensile strenght is required for these three formulations and is if there is a difference between the three formulation concercing required tensile strength. Or where can I find this in the literature?

Another question I have is, if it is possible that mebendazole and metformine show elastic behavior (or elastic recovery) at high compression forces.

Thanks in advance!

I want to create a complex of dimetformin and copper(2+) from this article ( ) , but I cannot set bond lenghts (from table 2 (last string)), because when I change lenght of bond in "cyclically bound" atoms, I cannot fixate already specified bond lenghts, they change when I try to change next one.

Is there any way to create a molecule fully with already setted up bond lenghts?

Or there are any other software, where I can make it easily?

Thanks!

Have been trying to get metformin to elute later than wave/solvent front on a Poroshell 120 C18 2.1x50x2.7. Tried with mobile phases, 0.1% formic acid with ACN + 0.1%FA, 0.1% FA with ACN and 10mM ammonium acetate with ACN. Tried isocratic and gradient elution. Thanks

In diabetic patients, the insulin diet should include a base insulin(e.g NPH or Lantus) and a short or fast insulin(e.g Apidra). But sometimes metformin is prescribed instead of fast-acting insulin. what is the reason?

How a mutation in introns affect the gene expression. if a SNP is not present in any downstream regulatory elements but in somewhere intermediate region of intron and how those polymorphism differentiate a response of those patients against drugs? eg. How rs7903146 polymorphism in TCF7L2 gene lead to risk of T2DM and how they differentiate in response against drugs like metformin or gliptin?

Hello,

I am working on a project which focuses on drug delivery using liposomes.I want to test the same on MCF-7 Breast cancer cell line,the effect of combination of cyclophosphamide and metformin on the cell line.

There are several clinical results suggesting that metformin is beneficial to prevent the formation of cancer tumors, but at least one result (see below) indicates that metformin can cause endoplasmatic stress and mitochondrial swelling, resulting in the possible impairment of calcium signaling related to the apoptosis of abnormal cells.

Sci Rep. 2017 Jul 11;7(1):5040. doi: 10.1038/s41598-017-05052-2.

The energy disruptor metformin targets mitochondrial integrity via modification

of calcium flux in cancer cells.

Loubiere C(1)(2), Clavel S(1)(2), Gilleron J(1)(2), Harisseh R(3), Fauconnier

J(4), Ben-Sahra I(5), Kaminski L(1)(2), Laurent K(1)(2), Herkenne S(6)(7),

Lacas-Gervais S(8), Ambrosetti D(9), Alcor D(1)(2), Rocchi S(2)(10), Cormont

M(1)(2), Michiels JF(9), Mari B(11), Mazure NM(12), Scorrano L(6)(7), Lacampagne A(4), Gharib A(3), Tanti JF(1)(2), Bost F(13)(14).

Author information:

(1)Inserm U1065, C3M, Team Cellular and Molecular Physiopathology of Obesity and Diabetes, Nice, France.

(2)Université Nice Côte d'Azur, Inserm, Nice, France.

(3)Inserm U1060/ INRA 1235/ Université-Lyon1/ INSA, Lyon, France.

(4)Inserm U1046, UMR CNRS 9214, Université de Montpellier, Montpellier, France.

(5)Northwestern University, Chicago, IL, USA.

(6)Department of Biology, University of Padua, Padua, Italy.

(7)Dulbecco-Telethon Institute, Venetian Institute of Molecular Medicine, Padua, Italy.

(8)Centre Commun de Microscopie Appliquée, Université de Nice Sophia-Antipolis, Nice, France.

(9)Centre Hospitalier Universitaire (CHU) de Nice, Hôpital Pasteur, Laboratoire

Central d'Anatomo Pathologie, 06002, Nice, France.

(10)Inserm U1065, C3M, Team Biology and pathology of melanocyte cells: From skin pigmentation to melanomas, Nice, France.

(11)CNRS, Institute of Molecular and Cellular Pharmacology, Sophia Antipolis,

France.

(12)Institute for Research on Cancer and Aging of Nice, CNRS-UMR 7284-Inserm U1081, University of Nice Sophia-Antipolis, Centre Antoine Lacassagne, Nice, France.

(13)Inserm U1065, C3M, Team Cellular and Molecular Physiopathology of Obesity and Diabetes, Nice, France. bost@unice.fr.

(14)Université Nice Côte d'Azur, Inserm, Nice, France. bost@unice.fr.

Mitochondrial integrity is critical for the regulation of cellular energy and

apoptosis. Metformin is an energy disruptor targeting complex I of the

respiratory chain. We demonstrate that metformin induces endoplasmic reticulum (ER) stress, calcium release from the ER and subsequent uptake of calcium into the mitochondria, thus leading to mitochondrial swelling. Metformin triggers the disorganization of the cristae and inner mitochondrial membrane in several cancer cells and tumors. Mechanistically, these alterations were found to be due to calcium entry into the mitochondria, because the swelling induced by metformin was reversed by the inhibition of mitochondrial calcium uniporter (MCU). We also demonstrated that metformin inhibits the opening of mPTP and induces mitochondrial biogenesis. Altogether, the inhibition of mPTP and the increase in mitochondrial biogenesis may account for the poor pro-apoptotic effect of metformin in cancer cells.

DOI: 10.1038/s41598-017-05052-2

PMCID: PMC5506014

PMID: 28698627

Why is metformin still prescribed for patients who can afford better drugs?

P.s.: I'm not a M.D.

As you know poly cystic ovaries and infertility is difficult to control in many cases. Sometimes prescribing traditional hormonal drugs and metformin in over weight female with NIDDM is not effective. What is the best therapeutic agents to control these patients?

Hi all,

I'm looking to convert a Cmax value for the drug metformin to a Cmax value to use in nude mice for an experiment. Is this possible? I have not been able to find the Cmax value of metformin in nude mice and need it for experimental planning.

animal is induced using stz (40 mg/kg) and nad(110mg/kg). when we checked the fasiting blood glucose one day it has decreased week later it has increased. pls clarify.

3 days after the induction of the dibetes using nicotinamide (110mg/kg) and streptozotocin(40mg/kg) the animal blood glucose was checked and it was treated with metformin(300 mg/kg). Glucose check was done for every 7 days with animal being fasted for 6 hours. first week FBG was found to be 168, 100 and 274. Metformin treatment was continued.   after one week when animal checked with fasting blood glucose again it showed 600+.

I am going to investigate the effect of metformin on antioxidant status and changes in proteins and membrane lipids in red blood cells in BDL-induced cholestatic rats.

Hi,

I have been treating my A549 cells with loads of drugs such as geftininb, erlotinib,metformin among others. Although only the cells that are in the 96 well plate are treated, but not the ones in cell culture flasks.

I believe that my cells have become drug resistant. The ic50 after 72 hours treatment were as follows:

Erlotninb (100 um)

geftininb (30 um)

Imatininb (30 um)

metformin (20 um)

Please let me know how can I see if they are indeed drug resistant apart from MTT assay for cell viability?

Acarbose or pioglitazone which will be more effective for diabete

Hey Guys,

I'm culturing cancerous breast tissue cells in vitro. Today I took the 24 well plate out of the incubator, and, being done with the cells, I sprayed bleach in all 24 wells. Instantly, half of the wells turned a deep yellow and the other half did not react (change color) at all. The cells that did react were in normal media where the cells that did not react had metformin (a common diabetes drug) in the media. Has anyone every heard of this? Please help me out even if its just a guess or opinion.

I conducted a short 5 day investigation exposing Mtilus edulis to Metformin concentrations (0ug/l, 100ug/l, 200ug/l, 500ug/l). I examined 1 specimen from day 1-4 from each variable and weighed both valves and flesh separately, on the final day I examine 5 mussels from each variable, and calculated an average.

Im wandering what statistic test to use to see whether there is 

a) significant difference between flesh weight and concentration of Metformin

b) significant difference between flesh weight and exposure period 

My data is as followed:

Day   |   0ug/L   |    100ug/l    |   200ug/L    |    500ug/l    |

1       |  1.5228  |   1.3204      |  1.6752       |  1.7080       |

2       |  0.9936  |   1.2145      |  1.3162       |  1.3493       |

3       |  1.3746  |    1.0422     |  0.8382       |  1.1621       |

4       |  1.4998  |   0.8381      |  0.8825       |  0.8212       |

5       |  1.1816  |  0.7263       |   0.7547      |   0.8747      |

-Values being flesh weight (g)

-Day 5 being an average of the 5 specimen examined

Thanks for the help! 

I want to hydrophobize Metformin HCL before encapsulation into the solvent with the micelle to prepare nanoparticles,

A 28 years old lady, height 5 feet, weight - 70 kg has been trying to conceive for the last on and a half years. She has a  32-33 days' menstrual cycle. Husband's semen analysis, follicular study and HSG reports are normal. Ultrasound of pelvis reveals evidence of polycystic ovaries with normal sized one ovary and other of 11 cc. She has been put on Tab Metformin 500 mg three times a day and Chirocyst by another Gynaecologist. She gives H/O partial seizures and is on Tab Orcabezapine. The patient uses Ovulation predictor kit to time intercourse. She used it on 14th and 16th day of the present cycle. The menstrual period got overdue by 6 days, yesterday. The patient used the Ovulation predictor kit and the result was positive. Today, she had a normal period. This is the first time that she had a delayed period. The query is, can ovulation predictor kit show positive result just one day prior to the onset of the menstrual period? Do the drugs she is taking interfere with LH levels?

In general, insulin is the preferred treatment for hyperglycemia in hospitalized patients previously treated with oral agents. However, there are some circumstances where insulin may not be necessary, it could maintain oral antidiabetic?

Reading some research recently on the anti-diabetic drug metformin and its mode of action I wondered if there were many explanations about its effect on Alzheimers patients ? Looking at the biochemistry around the drug I thought of other possible explanations for its effects.