Imeglimin. A new and novel drug thats better than Metformin

#61

Yes, it was odd because I had been taking metformin for decades. I refused to think that the diarrhea was caused by the metformin. It is a known side effect. Thinking it was a coincidence, I started and stopped metformin several times, allowing some time between tests. Same result every time. One 500 mg metformin ER tablet, even taken with a large meal, causes me to have diarrhea for two to three days. I have no idea why my body no longer tolerates metformin.

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#62

Though Claude says this after I uploaded my latest lab report.

“Your metabolic panel is remarkably clean for an 85-year-old. Liver function (AST 16, ALT 14, alkaline phosphatase 53, bilirubin 0.5) is excellent — no hepatic concern for any of the drugs we’ve been discussing. Your lipids are extraordinary: total cholesterol 109, LDL 41, ApoB 53. Whatever you’re doing there is working extremely well. HbA1c of 5.4% is in the fully normal range, which is striking given that your fasting glucose was 107. TSH is normal, iron studies normal, thyroid fine.”

The Clues About Metformin Intolerance
The BUN/Creatinine ratio is the most interesting finding here. Your creatinine is 0.96 — which looks normal — but your BUN is 33 (high), giving a BUN/creatinine ratio of 34, well above the normal ceiling of 22. A chronically elevated BUN/Cr ratio in the absence of obvious dehydration or GI bleeding often reflects either a high-protein diet, or more relevantly, reduced renal tubular function that isn’t yet captured by the creatinine or eGFR alone.
Your eGFR of 78 puts you in CKD Stage G2 (mildly reduced). However, eGFR calculated from creatinine tends to overestimate true GFR in elderly men with reduced muscle mass, because creatinine is a byproduct of muscle metabolism — less muscle means less creatinine produced, which flatters the eGFR number. At 85, your true functional GFR may be meaningfully lower than 78. This matters enormously for both metformin and imeglimin.

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#63

Hi Desert and others, From another group I hear from the Gut experts that poly pharma (etc) can up regulate the gut/vegas nerve where you (me) can move to a hair trigger gut re motility.

I can’t trace back which pill or combo did it for me but I can have periods of mild IBS. I theorize if I stopped all my pills my IBS would subside. ;( ;( ;(

AND I take quiet a bit of oral KPV, BPC-157, lazaritide, l-glutamine to quiet and heal the gut. AND that could be also apart of the problem! Pills to fix pills rarely works long term.

I no longer can take even a small amount of creatine (mono or hcl) without diahrea. Even the fixer l-glutamine can be a problem.

I’ve had a life time of reactivity, MCAs , alergies so it appears my proneness to be over reactive is in play.

Desert, I’ve thrown the kitchen sink at trying to calm my gut to no avail. I have difficulty taking my own advice of: stop all / most pills (a generalizism) an give a period of time to quiet the whole bodies proness to over reacting. Just a theory I can’t manage to follow.

Best of luck, curt

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#64

For anti aging I added dapaflozen (??) an SGLT2, 10mg AM, and may not be getting the most out of taking this by takiing in AM vs in front of food.

Talk here of taking imeglimin WITH metformin any thoughts of imeglimin with a SGLT-2?

tnx to all, curt

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#65

Deborah, we are similar. My A1c is 5.6, my FBS is 92, and my fasting insulin is 2 -4 (I’m an omnivore). My c-peptide is 1.5. I am also taking 1g of Metformin. By all accounts, it seems I have some beta-cell insufficiency and a slow phase 1 insulin response. Have you done any genetic analysis? I did. Using my 23andMe data and running it through Rhonda Patrick’s genetic service I learned that I have several variants that predispose me to diabetes: SLC30A8, IRS1, ACE, CRY2. The first is a zinc waster, which means I don’t absorb zinc well and zinc is necessary to produce insulin. Sure enough, I tested on the low end of normal. I have upped my zinc and we will see it’s impact in upcoming tests. My IRS1 variant impairs insulin signaling and could be ameliorated by reducing saturated fat (at least according to Rhonda’s site). If you haven’t already, a genetic analysis could provide some interesting data for you. I will be ordering Imeglimin from Maulik soon, too. And thanks to Charles for alerting me to the possibility of Met/Imeg combo therapy. BTW, have you tried this glucose metabolism calculator? It provides some interesting metrics that were new to me. Glucose Metabolism Interpreter.

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#66

Thanks for your post, Kebossit. A while back I did do the Rhonda Patrick report on my 23&Me data. Just revisited it, and it showed a low adiponectin level, and a risk of obesity. The obesity risk was also highlighted in my Promethease report. This confirms what I have long felt was true – I gain weight so easily and have to watch calories very carefully – while also needing to work extra hard, and find low-calorie high protein nutrition to grow some muscle. The Rhonda Patrick report also highlighted a tendency to develop diabetes. So this, combined with the recent insights that genetics control about half – much higher than previously thought – of your health/longevity: a giant “Oy vay,” as they say.

This is all so discouraging, but knowing is better than not knowing. When I have told people that my mother is 99 (but very severely demented) and my grandmother lived to 103, they respond “You’ve got great genetics.” NOT! Could be worse, but I do not want to be a skinny, frail, demented centenarian.

If it were not for this forum, I would likely still be blithely believing I was quite OK doing what I was doing, which wasn’t nothing but: now I know I need to work much harder. So, even though rapamycin in particular does not seem to be an intervention that is matched with my body or my genes, (or my age) I have learned so much, and confirmed so much that I already sensed but could not verify until now. Thank you all!

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#67

Ya, I also have low adiponectin and an obesity gene (FTO) per Rhonda. I am curious why you don’t think rapa would work for you…especially since we seem to have some similar genes and maybe age (I am 59 on Saturday). Low muscle mass? It is on my to-do list.

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#68

I had similar problems with lower digestive tract problems and occasional bouts of unexpected diarrhea. This was after I stopped taking metformin, which acts as a strong laxative for me. May be an effect of polypharmacy or too many supplements. Old age is certainly a factor. When I was young, I had a cast-iron stomach that would tolerate most anything.

My first line of defense was to take 2 mg of loperamide daily. This is a safe dose for long-term use. This worked quite well, but didn’t address the underlying problem.

I eventually concluded that my gut bacteria might be a problem due to occasional antibiotic use, including the DAV protocol “Three-drug combination therapy for anti-aging.”

So, how to address the problem of gut bacteria? Some forum members suggest eating a lot of yogurt, as well as kimchi and sauerkraut. I think that is a good suggestion, but I don’t like any of them.

My solution, which is working quite well, is to take probiotics daily. I have tried them occasionally in the past and was not impressed. But I think I was using the wrong protocol.

The key, from my experience, is to take the probiotic if it is not already in an enteric-coated capsule and put it in a slightly larger enteric-coated capsule. Gut bacteria need sufficient fiber to thrive. I don’t get enough fiber in my protein-weighted diet. I cannot tolerate most fiber supplements, such as inulin, because they cause a lot of gas. I use “Advanced Acacia Fiber Powder, Organic Soluble Fiber Leaky Gut Repair Powder.” Natural Supplement Prebiotic for Gut Repair" from Amazon. I really like this fiber because it dissolves in my coffee without adversely affecting the taste.

My protocol is not medical advice. Just the result of an N=1 experiment.:

So, I have solved the problem for me. Take any good probiotic bacteria supplement; I really don’t think it matters. I would start with a known good bacteria that is often prescribed for children, Lactobacillus Breve. I started with this and had very good results. You must take it in an enteric-coated capsule to see results within a reasonable amount of time. It takes about 30 days to see results from a probiotic supplement, along with a daily dose of fiber. You can take loperamide daily while you are doing this. It has no adverse effects on the gut bacteria.

Claude:

General Safety of Low-Dose Daily Use

For mild, chronic loose stool issues, low-dose daily loperamide is actually commonly used and considered reasonable in several clinical contexts:

  • Crohn’s disease: It’s frequently used as an adjunct for mild functional diarrhea, but with an important caveat — it should generally not be used during active flares or if there’s any risk of toxic megacolon (a serious complication). During remission or for residual loose stools, it’s often appropriate.
  • Polypharmacy/supplement-induced loose stools: This is a very common and generally safe application for loperamide, as the cause is functional rather than inflammatory.

Key Considerations

Dose: 2 mg/day is a low, conservative dose (the typical acute dose is 4 mg initially, then 2 mg after each loose stool, up to 16 mg/day). So 2 mg daily is well within a safe range for most people.

Drug interactions matter: Since polypharmacy is already a factor, it’s worth flagging that some medications (like certain antifungals, antibiotics like clarithromycin, or HIV medications) can raise loperamide blood levels and increase cardiac risk — though this is mainly a concern at higher doses.

Supplement interactions: Some supplements (like grapefruit-related compounds or St. John’s Wort) can affect how loperamide is metabolized.

When NOT to use it:

  • During a Crohn’s flare with significant abdominal pain or fever
  • If the diarrhea may be from an active infection (C. diff, for example)
  • If there’s blood in the stool

Long-term use: Regular use can sometimes mask underlying problems that need attention, so it’s worth periodically reassessing why the loose stools are happening rather than just controlling symptoms indefinitely.

Bottom Line

For the scenario you describe — mild, non-inflammatory loose stools in the context of Crohn’s (not actively flaring) or polypharmacy effects — 2 mg of loperamide daily is generally considered a safe and reasonable approach by most gastroenterologists. It’s not habit-forming and doesn’t carry significant systemic risk at that dose.

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#69

There was a time when I had gut issues and nothing seemed to work. What cleared it up were oregano pills. I read about it somewhere online and didn’t really expect it to work but in about a week’s time I had significant improvement.

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#70

Good question. I am curious about this also.

So, here is the prompt I gave to Google Gemini 3 Pro:

Role: pharmacist and longevity researcher. Task: identify and summarize research papers from the past 5 years that cover simultaneous dosing imeglimin with a SGLT-2 inhibitor, isolating the claims made in these papers.
Part 3: Claims & Verification

  1. Extract Claims: Identify every specific biological, medical, or protocol claim made in the study.
  2. Verify Externally: Search for “[Claim] meta-analysis”, “[Claim] Cochrane review”, “[Claim] RCT”.
  3. Assess Hierarchy of Evidence: Evaluate support using this strict hierarchy:
    • Level A: Human Meta-analyses / Systematic Reviews.
    • Level B: Human RCTs.
    • Level C: Human Observational / Cohort Studies.
    • Level D: Pre-clinical (Animal/In vitro). Flag heavily if claim relies on this level.
    • Level E: Expert Opinion / Anecdote.
  4. Detect Translational Uncertainty: If a claim is based on mouse/worm/yeast data but presented as human advice, label this as a “Translational Gap.”

STRICT CITATION PROTOCOL (MANDATORY):

  • Hyperlink Syntax: Use inline Markdown hyperlinks: Title (Year).
  • Verification: Do not generate a URL unless you have accessed the live webpage. Fallback to Title (Year) if the direct link is unstable.
  • Search Query: For every claim, execute: “[Topic] study [Journal Name] [Year]”.
  • Link Validation: Prioritize nlm.nih.gov, doi.org, nature.com, science.org. If no link is found, state “Source unverified in live search.”

Output Constraints:

  • Use Markdown formatting.
  • Do not use LaTeX, python code, or special characters that break simple text parsers or reveal formatting codes, etc…
  • Tone: Objective, critical, “Tell it like it is.” No hype.

Output: Provide a bulleted list of claims with their associated Evidence Level (A-E) and supporting external citations.

Gemini 3 Pro Response:

Claims & Verification: Imeglimin and SGLT-2 Inhibitor Co-Administration

The following claims regarding the simultaneous dosing of imeglimin and SGLT-2 inhibitors are extracted from literature published between 2021 and 2026.

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#71

Just started today, 2x 1000mg

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#72

Is anyone pairing this with retatrutide? Curious to hear about experiences.

Claude seems to think these would be synergestic, and in my opinion, Reta + SGLT-2 + imeglimin is probably a much more beneficial stack than whatever crazy & expensive things other biohackers are carrying out (e.g. reta + tesamorelin — which is probably the safest among the other crazy stuff going on in that space).

Excerpt of chat with Claude:

" Here’s the reasoning for why imeglimin (the “glimin” class oral antidiabetic, approved in Japan) could complement retatrutide (Lilly’s GIP/GLP-1/glucagon triple agonist):

Complementary mechanisms

Retatrutide acts at the receptor level — it agonizes GLP-1R, GIPR, and GcgR to drive weight loss, improve incretin signaling, and increase energy expenditure. Imeglimin works at the cellular/mitochondrial level, amplifying glucose-stimulated insulin secretion and preserving β-cell mass, while also enhancing insulin action in the liver and skeletal muscle PubMed Central. These are largely non-overlapping targets.

Countering retatrutide’s glucagon-driven hepatic glucose output

This is arguably the most compelling rationale. Retatrutide’s glucagon receptor agonism is intended to increase energy expenditure and lipolysis, but glucagon also stimulates hepatic gluconeogenesis — a potential glycemic liability. Imeglimin directly targets excess hepatic gluconeogenesis as one of its three core mechanisms PubMed Central, which could offset this side effect of glucagon agonism.

β-cell protection

Retatrutide drives sustained metabolic stress (weight loss, altered fuel partitioning). Imeglimin’s mitochondrial mechanism — rebalancing respiratory chain activity and reducing reactive oxygen species — preserves β-cell mass and function PubMed Central, which could support long-term durability of glycemic benefit.

Additive glucose-dependent insulin secretion with low hypoglycemia risk

Like GLP-1 receptor agonists, imeglimin enhances insulin secretion in an exclusively glucose-dependent manner, but their mechanism of action at the cellular level diverges PubMed — imeglimin works through NAD⁺/ATP amplification rather than receptor signaling. So combining them adds two independent glucose-dependent insulin-secretion pathways without substantially increasing hypoglycemia risk.

Residual insulin resistance

Retatrutide’s primary benefit is weight-mediated metabolic improvement. But imeglimin targets multiple mechanisms — increasing insulin sensitivity, decreasing gluconeogenesis, increasing β-cell function, and improving mitochondrial function PubMed Central — potentially addressing insulin resistance that persists beyond what weight loss alone corrects."

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#73

@shc I agree re reta + imeg + sglt2 and I’ve been doing GH secretagogs early AM and before bed: Ipamorelan 300mcg + CJC 300 mcg + tesamorlan 300mcg. I agree prob too much pressure from secretagogs. Its said that your body can only respond with so much GH release from the secretagog input and anything more then your body can put to use is wasted. Per my costs so low I con’t care about wasting a peptide. IE nexaph.com and chinese places another 20% cheaper.

I’m 72yo male, fit and no GH secretagogs my IGF-1 is just 159, 2 hr after this dose my IGF-1 is 250 and has seen higher. So the rule that GH secretagogs loose effectiveness above age XX is maybe true in general but the healthiier you are the more you work on rebuilding your organs, pineal gland, thymus via the various bioregulators; epitalon, pinealon, chronuluten, vesugen, vilon, livagen, cartalax cortagen, et al (they have some cross talk) the more you get your organs to still produce as I’ve have tested to show.

I just need to share from the body builder / health groups that there are some 20% of non responders to Reta and they have to move back to Tirzepatide. Side effects reported can be: hyper to hypo glucose even early AM during sleep. Papitation, tacacardia at night, even an increase in appitite which is more often then reduction. So some folks combine semaglutide or tirzepatide with reta. Some lower percent up to 50/50 to reta.

Just reporting that 100% reta can be tolerated by alot of folks, some do have to swap to tirz or combine with sema or tirz.

I’ve heard that if you are on 3mg/week in multiple doses tirzepatide that reta might need 4mg. IMHO though I’d still swap mg for mg onto reta and titrate up as you search for results.

I do 1mg / week 50:50 tirz and reta not for weight loss but for HRT a forever protocol.

Another issue: GLP-1’s interact with mitchondria function along with MANY other compounds: SLU-PP-332, 5amino-1q, even Urolithin-a, SS31, MOTSC and prob many other compounds. Meaning you may without knowledge amplify the effect of reta by adding some seemingly unrelated compound and now you have side effects, nausia, total constipation by adding an unrelated compound but under the hood there IS a connection.

The single common thread to me is lower doses of everything and very very careful titration up ideally just one thing at at time and give a month for the connectedness to settle out. I wish this was all simpler but its not.

Good luck, curt

PS hate to not mention, its common wisdom in the health coach circles that all this is useless completely and practically useless if ALL of your hormones are not up to 40yo levels: E, P, testosterone and free-T3 above 3.2 etc etc etc. I will add that fasting glucose and insulin needs to be well under insulin resistant. GLP-1 is NOT a cure for insulin resistance as is marginally wrongly touted. Get your diet fixed THEN GLP-1. I can share cheap blood testing and mail order T, E, P hormone sourcing with just an emailed blood test. Thyroid, ideally is NP thyroid a desicated till needs a local prescriber.

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#74

Alone for replace metformin? Or with met, acarbose, sglt2, etc.

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#75

Just noticed this message from a while back… here is the response from Gemini 3 Pro:

Contraindication Analysis: Imeglimin and Rapamycin (Sirolimus)

There is currently no scientific or clinical evidence indicating that imeglimin is contraindicated for individuals taking rapamycin. On the contrary, existing pharmacokinetic and pharmacodynamic data suggest the two compounds are structurally independent and potentially synergistic in mitigating the metabolic side effects of mTOR inhibition.

Pharmacokinetic (PK) Independence

The primary safety concern when stacking compounds with rapamycin is the modulation of cytochrome P450 3A4 (CYP3A4), as rapamycin is heavily dependent on this enzyme for hepatic metabolism.

  • Renal Excretion vs. Hepatic Metabolism: Imeglimin is excreted largely unchanged in the urine via active renal secretion (utilizing OCT1/OCT2 and MATE transporters). It undergoes minimal hepatic metabolism.
  • Absence of CYP Interference: In vitro and in vivo human studies confirm that imeglimin has no significant induction or inhibition potential toward CYP450 enzymes, including CYP3A4. Therefore, co-administering imeglimin will not artificially elevate or depress systemic rapamycin trough levels, avoiding acute toxicity or sub-therapeutic dosing.

Pharmacodynamic (PD) Synergy

Rapamycin is utilized in longevity protocols to inhibit the mTORC1 pathway, a mechanism that reliably delays cellular senescence but frequently induces metabolic toxicity. Long-term sirolimus use dampens peripheral insulin signaling and increases hepatic gluconeogenesis, often resulting in insulin resistance, hyperglycemia, and hypertriglyceridemia (clinically documented as New-Onset Diabetes After Transplantation, or NODAT).

Imeglimin presents a compelling mechanistic countermeasure to this specific side-effect profile:

  • Mitochondrial Rescue: Rapamycin-induced insulin resistance is driven by peripheral tissue metabolic stress. Imeglimin targets mitochondrial bioenergetics (mildly inhibiting Complex I while stimulating Complex II), reduces reactive oxygen species (ROS), and upregulates glucose-stimulated insulin secretion without exhausting $\beta$-cells.
  • Clinical Application for mTOR Toxicity: Recent clinical reviews explicitly identify medications targeting compromised mitochondrial function, specifically citing imeglimin, as therapeutic interventions to rescue blood sugar control and metabolic homeostasis in patients suffering from immunosuppressant-induced diabetes (including those on sirolimus).

Knowledge Gaps & Required Data

While informed speculation strongly supports the safety and metabolic utility of this combination, significant evidentiary gaps remain in the literature.

  • Translational Void: There are zero Randomized Controlled Trials (RCTs) directly evaluating the co-administration of imeglimin and rapamycin in healthy human populations for healthspan extension or sarcopenia prevention.
  • Data Requirements: To definitively validate this protocol, crossover clinical trials are required. These studies must quantify whether imeglimin’s activation of upstream metabolic sensors (such as Akt or AMPK) unintentionally blunts rapamycin’s geroprotective mTORC1 suppression at the skeletal muscle or organ level. Furthermore, continuous glucose monitoring (CGM) and cross-sectional lipid tracking in a co-administered cohort are required to quantify the exact magnitude of imeglimin’s rescue effect on rapamycin-induced dyslipidemia.
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#76

Imeglimin Shows Sustained Real-World Efficacy in Aging Diabetics, But High-Dose Metformin Combo Triggers Gut Distress

Mitochondrial modulators are gaining traction in the longevity and metabolic health space, and imeglimin—a novel oral tetrahydrotriazine—is showing promise outside of strictly controlled clinical trials. A new retrospective cohort study analyzed the 12-month real-world efficacy of imeglimin in individuals with type 2 diabetes. The drug, which targets mitochondrial complex I to enhance insulin secretion and suppress hepatic gluconeogenesis, effectively reduced HbA1c by an average of 0.8% across all age groups over the study period.

Crucially for longevity protocols targeting older demographics, imeglimin maintained its efficacy and favorable tolerability profile in the very elderly, including those aged 75 and older. However, the data revealed a significant translational caveat for combination therapies: co-administering imeglimin with high-dose metformin (1,000 mg/day or more) significantly increased the frequency of gastrointestinal disturbances. Because both drugs inhibit mitochondrial complex I and share structural similarities, their stacked use likely amplifies gut toxicity. Patients whose biguanide doses were reduced or discontinued when starting imeglimin experienced fewer GI events, but they also saw less robust HbA1c reductions compared to those who maintained their biguanide dose, highlighting a stark efficacy-versus-tolerability trade-off.

Beyond glycemic control, the study noted favorable off-target metabolic effects. Over 12 months, subjects exhibited significant reductions in body weight, triglycerides, and liver enzymes, specifically ALT, AST, and gamma-GTP. These secondary outcomes suggest imeglimin may possess hepatoprotective properties, potentially offering a therapeutic vector against metabolic dysfunction-associated steatotic liver disease (MASLD), a major driver of systemic aging.

  • Paper: Real-world effectiveness and safety of imeglimin: a single-center retrospective cohort study in Japan
  • Context: This research was conducted by scientists at the Central Japan International Medical Center, Gifu University, and Kyoto University in Japan.
  • Journal: It was published in Frontiers in Clinical Diabetes and Healthcare.
  • Impact Evaluation: The impact score of this journal is 2.2, evaluated against a typical high-end range of 0–60+ for top general science, therefore this is a Low impact journal.
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#77

Looking at imeglimin literature, I was currently focusing on the effect on mitochondria, and a few papers were interesting enough to share here in a batch (with brief commentary from me).

There has been talk here about imeglimin vs metformin in regard to exercise, and a question about the possibility that imeglimin might be similarly suboptimal in the context of exercise. It seems not. In fact, there might be synergies between imeglimin and exercise - at least resistance exercise (free article).

Combination of imeglimin and resistance exercise improves mitochondrial function and glucose metabolism in skeletal muscles

“These findings suggest that the combination of imeglimin and RT [Resistance Training] is a promising therapeutic approach to enhance mitochondrial function and glucose metabolic capacity.”

There have been suggestions that some drugs that were used in T2DM were actually beneficial for CV health, such as SGLT2i. Well, it looks like perhaps imeglimin might join the club, insofar as it might mitigate atherosclerosis - who knew!

Molecular mechanism for pancreatic β-cell dysfunction and atherosclerosis

“Recently we have reported that imeglimin exerts beneficial effects on mitochondria morphology in β-cells and/or number and quality of insulin granules. In addition, we have reported that imeglimin shows favorable effects against the development of atherosclerosis independently of glycemic and lipid control.”

That part about the effect on atherosclerosis was independent of glycemic and lipid control is very important, because it tells us that this effect is not solely due to imeglimin being an anti-diabetic agent, and also because it can be used as an addition to LLT (statins, ezetimibe etc.), and the effects on atherosclerosis should therefore stack.

How does imeglimin work in beta cells? Overview.

Current understanding of imeglimin action on pancreatic β‐cells: Involvement of mitochondria and endoplasmic reticulum homeostasis

A big part of fighting aging is centered around the inflammatory process that is downstream from LPS propagation. It looks like imeglimin might be helpful here (free article).

Imeglimin attenuates NLRP3 inflammasome activation by restoring mitochondrial functions in macrophages

“We demonstrated for the first time that imeglimin reduces LPS-induced NLRP3 inflammasome activation by inhibiting mPTP opening in THP-1 macrophages. These results suggest that imeglimin could be a promising new anti-inflammatory agent for treating diabetic complications.”

The next paper speaks for itself - mitochondrial ROS is a fundamental driver of aging, so it’s nice to see imeglimin might be helpful here (free article).

Suppressing Mitochondrial ROS Production is Beneficial in Multiple Preclinical Models of Human Disease

Finally, the last paper is just a case report, but I liked it because it used three classes of drugs, which many of us have an interest in: SGLT2i, ARB and glimin. As a small additional factor, the ARB in question is olmesartan which I have increasing interest in.

Mitochondrial Nephropathy With m.5538G>A Mutation Within the tRNA-Trp Region Assessed by Mitochondrial Function Analysis: A Case Report

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#78

I use acarbose 100mg each meal, dapa 10mg and tirz 3mg + the imeglimin

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