Glucophage/Metformin Info

Glucophage – by Big A

Glucophage is the brand name for metformin hydrochloride.

Metformin is NOT oral insulin. People confuse it as such, because in most countries oral insulin is called Diamicron and metformin is called Diaformin.

When your body releases insulin, over time, your insulin receptors get 'dull', less responsive. In advanced stages that becomes type II diabetes.

Metformin 'refreshes' those receptors, making them more sensitive to the insulin that your body releases.

It is a great product. Taken straight after a large meal, within the hour you will have EXTREMELLY full muscles. Dosages are 500mg after a normal to large carb meal, 1,000mg after a big carb meal and 1,500mg after all you can eat at Pizza Hut. You can take it after as many meals in a day as you wish, as long as those are large carb meals.

I generally found that if I take less than 100g of carbs for every 500mg metformin, I go into hypo. And yes, you can eat fat meals, as metformin will indirectly prevent the fat being deposited.

The long acting glucophage is taken before bed as it helps the person release less insulin throughout the night, especially if they had a big dinner like most people do. But that doesn't apply to a healthy person. That might get a healthy person in hypo overnight.

I believe every human should be on metformin, as it helps keep your insulin receptors fresh and as such it will prevent type II diabetes.

xcel

I was in keto when i took 1000mg of gluco before bed...
I'm still alive and healtier! Glucophage doesn't cause hypoglicemy!
1- Gluco shut down your endogenus slin levels (the more slin-sensitivity, the less slin required)
2- Gluco blocks carbs absorption at intestinal level
3- Gluco inhibits gluconeogenesis
4- Gluco enhance slin receptor sensitivity
5- Gluco allows the body to produce more slin receptors

this means that gluco can't do a carbs muscle loading if used alone, there aren't enough carbs and slin in your body to do this (see 2 and 3); the best way to do this, is a load/download diet regimen, with gluco in carbs download days and slin in load days.

remember: gluco is an antihyperglicemic drug, it isn't a macronutrients partitioning agent (as slin does)

JM2C

this is an interesting study abuot met and human androgens levels...

Effects of short term metformin administration on androgens in normal men.

Shegem NS, Nasir AM, Jbour AK, Batieha AM, El-Khateeb MS, Ajlouni KM.

National Center for Diabetes Endocrinology and Genetics, Jordan University Hospital, Amman, Jordan.

OBJECTIVE: To study the effect of metformin on androgens in normal men. METHODS: A total of 12 healthy males volunteered to participate in the study. A blood sample was obtained from each of them and analyzed for the following: Testosterone (total and free), sex hormone binding globulin dehydroepiandrosterone sulphate, 17-hydroxyprogesterone, luteinizing hormone, and follicle stimulating hormone. In addition, each participant was subjected to a glucose tolerance test and his insulin level was measured. Metformin 850 mg twice daily for 2-weeks was given to each subject after which the above tests were repeated. A paired t-test was used to assess the statistical significance of any observed differences before and after metformin. RESULTS: After metformin administration, there was a significant reduction in serum level of total testosterone (p=0.0001), free testosterone (P=0.002), and 17 hydroxyprogesterone (p=0.0001). There was also a significant increase in serum level of sex hormone binding globulin (p=0.009) and dehydroepiandrosterone sulphate (P=0.0008). Serum levels of luteinizing hormone and follicle stimulating hormone showed no significant changes. Similarly, there were no changes in fasting plasma glucose, fasting serum insulin, weight, or blood pressure. CONCLUSION: Metformin administration was associated with a reduction in total testosterone, free testosterone, and 17-hydroxyprogesterone and an increase in sex hormone binding globulin and dehydroepiandrosterone sulphate in normal males.
The clinical significance of these findings needs further investigation.

glucophage is an insulin-lowerig agent...

Treatment of polycystic ovary syndrome with insulin-lowering agents.

Glueck CJ, Streicher P, Wang P.

Cholesterol Center, ABC Building, 3200 Burnet Avenue, Cincinnati, Ohio, USA. [email protected]

Early diagnosis and therapy of the underlying insulin resistance of heritable polycystic ovary syndrome (PCOS), often manifested at menarche, facilitate the reduction and/or reversal of the reproductive and metabolic morbidity of PCOS, as well as reduce the risk factors for cardiovascular disease. PCOS is characterised by oligoamenorrhoea, clinical and biochemical hyperandrogenism, infertility, recurrent miscarriage, insulin resistance, hyperinsulinaemia, gestational diabetes, impaired glucose tolerance, Type 2 diabetes, morbid obesity, hypertension, hypofibrinolysis, hypertriglyceridaemia, low levels of high density lipoprotein-cholesterol and a sevenfold risk increase in cardiovascular disease. Insulin sensitising-lowering agents reduce insulin resistance and hyperinsulinaemia, reverse PCOS endocrinopathy and ameliorate the reproductive, metabolic and cardiovascular morbidity of the disorder. The largest literature on the subject discusses metformin. Improved pregnancy outcomes in women with PCOS receiving metformin may be attributed to its ability to reduce insulin resistance, hyperinsulinaemia and hypofibrinolytic plasminogen activator inhibitor activity by the enhancement of folliculogenesis and improvement of oocyte quality.

- glucophage has an activity of about 2 hours in our body (in healty subjects; with renal disfunctions it can reach 5 hours);
- it inhibits vit B12 absorption;
- it decreases VLDL levels;

JM2C

LONG TERM EFFECTS OF GLUCOPHAGE IN MUSCLES GLUCOSE DISPOSAL (BUT SOUND A LITTLE BIT STRANGE...)

Metformin increases AMP-activated protein kinase activity in skeletal muscle of subjects with type 2 diabetes.

Musi N, Hirshman MF, Nygren J, Svanfeldt M, Bavenholm P, Rooyackers O, Zhou G, Williamson JM, Ljunqvist O, Efendic S, Moller DE, Thorell A, Goodyear LJ.

Research Division, Joslin Diabetes Center, Brigham and Women's Hospital and Harvard Medical School, One Joslin Place, Boston, MA 02215, USA. [email protected]

Metformin is an effective hypoglycemic drug that lowers blood glucose concentrations by decreasing hepatic glucose production and increasing glucose disposal in skeletal muscle; however, the molecular site of metformin action is not well understood. AMP-activated protein kinase (AMPK) activity increases in response to depletion of cellular energy stores, and this enzyme has been implicated in the stimulation of glucose uptake into skeletal muscle and the inhibition of liver gluconeogenesis. We recently reported that AMPK is activated by metformin in cultured rat hepatocytes, mediating the inhibitory effects of the drug on hepatic glucose production. In the present study, we evaluated whether therapeutic doses of metformin increase AMPK activity in vivo in subjects with type 2 diabetes. Metformin treatment for 10 weeks significantly increased AMPK alpha2 activity in the skeletal muscle, and this was associated with increased phosphorylation of AMPK on Thr172 and decreased acetyl-CoA carboxylase-2 activity. The increase in AMPK alpha2 activity was likely due to a change in muscle energy status because ATP and phosphocreatine concentrations were lower after metformin treatment. Metformin-induced increases in AMPK activity were associated with higher rates of glucose disposal and muscle glycogen concentrations. These findings suggest that the metabolic effects of metformin in subjects with type 2 diabetes may be mediated by the activation of AMPK alpha2.

Don't know what's the meaning of this...

maybe i'm right

Metformin increases insulin-stimulated glucose transport in insulin-resistant human skeletal muscle.

Galuska D, Zierath J, Thorne A, Sonnenfeld T, Wallberg-Henriksson H.

Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden.

The effect of metformin (0.1 mM) on glucose transport was investigated in healthy control and in insulin-resistant human skeletal muscle. Muscle samples (200-400 mg) were obtained from the rectus abdominis muscle (abdominal surgery) or from the vastus lateralis portion of the quadriceps femoris muscle (open biopsy technique) from 8 healthy controls (age 38 +/- 4 yrs, BMI 23 +/- 1) and from 6 insulin-resistant subjects (age 53 +/- 5 yrs, BMI 30 +/- 2). Metformin had no effect on basal or insulin-stimulated (100 microU/ml) 3-0-methylglucose transport in incubated muscle strips from healthy subjects. Muscle tissue from the insulin resistant group did not respond to 100 microU/ml of insulin (0.73 +/- 0.17 for basal and 0.81 +/- 0.22 mumol x ml-1 x h-1 for insulin-stimulation, NS). Basal glucose transport was unaffected by metformin, whereas insulin-stimulated (100 microU/ml) glucose transport was increased by 63% in the insulin-resistant muscles (0.73 +/- 0.17 in the absence vs 1.19 +/- 0.18 mumol x ml-1 x h-1 in the presence of metformin, p less than 0.05). In conclusion, metformin abolishes insulin-resistance in human skeletal muscle by normalizing insulin-stimulated glucose transport accross the muscle cell membrane. The mechanism for this effect remains to be elucidated.

glucophage can't causes hypo...



Metformin: a review of its pharmacological properties and therapeutic use.

Hermann LS.

In a survey, the pharmacological and clinical documentation of metformin is presented and discussed, and the present state of knowledge relating to metformin-associated lactic acidosis is reviewed. The use of metformin in the treatment of diabetes is based on clinical experience over twenty years. It has been well documented that metformin is effective in maturity-onset diabetes both as monotherapy and in combination with a sulphonylurea. An advantage of metformin treatment is the tendency to weight reduction and the absence of significant hypoglycaemia; blood glucose levels are reduced only to normal. The disadvantages are the gastro-intestinal side effects and the potential risk of vitamin B 12 and folic acid deficiency during long-term use. Metformin-associated lactic acidosis is a very rare complication, which has mainly occured in patients with serious renal insufficiency or other contra-indications to the use of metformin. The association between phenformin and lactic acidosis has led to withdrawal of this biguanide in several countries. Metformin differs from phenformin in certain important respects, and the normal use of metformin does not involve the risk of side effects disproportionate to the intended effect. Further experimental studies are required to substantiate pharmacokinetics and metabolic effects of metformin in man.

henry said:

this is an interesting study abuot met and human androgens levels...

Effects of short term metformin administration on androgens in normal men.

Shegem NS, Nasir AM, Jbour AK, Batieha AM, El-Khateeb MS, Ajlouni KM.

National Center for Diabetes Endocrinology and Genetics, Jordan University Hospital, Amman, Jordan.

OBJECTIVE: To study the effect of metformin on androgens in normal men. METHODS: A total of 12 healthy males volunteered to participate in the study. A blood sample was obtained from each of them and analyzed for the following: Testosterone (total and free), sex hormone binding globulin dehydroepiandrosterone sulphate, 17-hydroxyprogesterone, luteinizing hormone, and follicle stimulating hormone. In addition, each participant was subjected to a glucose tolerance test and his insulin level was measured. Metformin 850 mg twice daily for 2-weeks was given to each subject after which the above tests were repeated. A paired t-test was used to assess the statistical significance of any observed differences before and after metformin. RESULTS: After metformin administration, there was a significant reduction in serum level of total testosterone (p=0.0001), free testosterone (P=0.002), and 17 hydroxyprogesterone (p=0.0001). There was also a significant increase in serum level of sex hormone binding globulin (p=0.009) and dehydroepiandrosterone sulphate (P=0.0008). Serum levels of luteinizing hormone and follicle stimulating hormone showed no significant changes. Similarly, there were no changes in fasting plasma glucose, fasting serum insulin, weight, or blood pressure. CONCLUSION: Metformin administration was associated with a reduction in total testosterone, free testosterone, and 17-hydroxyprogesterone and an increase in sex hormone binding globulin and dehydroepiandrosterone sulphate in normal males.
The clinical significance of these findings needs further investigation.

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It seems the testosterone lowering effects should be more then negated when one uses a gram or more of test a week. Just my opinion.........

would you see this being a problem for a type 1 diabetic. Insulin dependent?

i heard that metformin makes insulin unpredictable, and the two shouldnt be combined

I have been taking this stuff for about a week and a half. I really think it works. I can eat a really large meal and never feel bloated after. I do not use it as an excuse to cheat however. I stick to the diet very close. But I believe I am the type of person who may have a tendancy to become insulin insensitive, as my father is. So I cannot see any reason NOT to be on it.

I need more info. Anyone with any good experience please let me know. Once I have been on 6 months or so I will post my experience.

In studies, like above it has been shown to lower free test (raise shbg levels). If you're using steroids, then this isn't a big deal, but if you're not, I would look into this more before using it.

I haven't really noticed a drop in test. Maybe that takes a while. I just looked ripped in the mirror though.

I was planning on a long term, 6 month +, HgH cycle and my doctor recommended metaformin and armour thyroid throughout to augment the GH. Thoughts on it combined with GH....??

Anybody out there wish to comment??? please...... thanks

Alcatraz said:

I haven't really noticed a drop in test. Maybe that takes a while. I just looked ripped in the mirror though.

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What do you mean you haven't noticed a drop in test? Have you gotten bloodwork while on metformin?

do you guys think that taking metformin once a day after a large meal would give any results? or would it be better to use it at least 2 times a day? ok, last question i promise. how long should the metformin be used for? i guess what im asking is if i start it now, will i have to use it for the rest of my life? or would it be ok to just use during my cycles and what not? thanks in advance people.

I have not gotten any bloodwork done yet. I will in a couple weeks.

As to the other questions ironfreak, I am new to metformin. SO I really shouldn't comment on it yet. I think too many people do that on this board instead of just sitting back and letting the more educated guys answer. If I throw my two cents in it may just confuse the hell out of everybody.

Thanks

Alcatraz said:

I have not gotten any bloodwork done yet. I will in a couple weeks.

As to the other questions ironfreak, I am new to metformin. SO I really shouldn't comment on it yet. I think too many people do that on this board instead of just sitting back and letting the more educated guys answer. If I throw my two cents in it may just confuse the hell out of everybody.

Thanks

Click to expand...

lol thanks anyways man. i'm just afraid to start this without knowing 100% of what i'll be getting into. i eat huge amounts of carbs in almost every meal so i'm thinkin this stuff could really help. i'm gonna keep researching on it and reading more info but im leaning towards trying it.