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
EXTREMELY 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.
Glucophage doesn't cause hypoglycemia!
1- Gluco shut down your endogenous 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
- glucophage has an activity of about 2 hours in our body (in healthy subjects; with renal
dysfunctions it can reach 5 hours);
- it inhibits vitamin B12 absorption;
- it decreases VLDL levels;
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)
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.
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. firstname.lastname@example.org
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.
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
Research Division, Joslin Diabetes Center, Brigham and Women's Hospital and Harvard Medical School, One Joslin Place, Boston, MA 02215, USA.
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.
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
Metformin: a review of its pharmacological properties and therapeutic use.
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
hypoglycemia; 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.
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