• Lipo Mic Injection
  • Lipo Mic Injection

Overview Of Lipo (MIC) Injection

Dosage Power Of Lipo (MIC) Injection
Methionine / Inositol / Choline Chloride 25/50/50 mg/mL 10 mL Vial
Methionine / Inositol / Choline Chloride 25/50/50 mg/mL 30 mL Vial
Generic Details
Lipotropes are compounds that may aid in the breakdown of body fat by acting on lipid metabolism and synthesis pathways. When used in combination with lifestyle modifications such as exercise and diet, lipotropic compounds may promote fat and weight loss.

Lipotropic compounds including vitamins, nutrients, and other natural or pharmacological agents may be administered as injections or in the form of oral supplements. Injections provide the advantage of better bioavailability by avoiding enzymes in the gastrointestinal tract. In addition, injections may be especially beneficial in individuals with gastrointestinal absorption issues.

The lipotropic agents in this injection are methionine, inositol, and choline. While each may individually affect the mobilization of fats, the combination may provide synergistic benefits.The physiological role of each compound and the effects of supplementation are described below.


Methionine is a sulfur-containing branched-chain amino acid. A precursor for cellular methylation reactions, methionine plays an important role in lipid metabolism, polyamine synthesis, immune function, heavy metal chelation, and maintenance of redox balance.4 Conversely, dietary methionine restriction in rodents increased energy expenditure, improved insulin resistance, and enhanced lipolysis and fatty acid oxidation in adipose tissue.5

The lipotropic effects of methionine may be attributed to its metabolite S-adenosyl methionine (SAM). SAM is synthesized from methionine via an energy-consuming reaction. SAM administered orally or by injection has been investigated as a treatment for liver diseases, osteoarthritis, and depression.6 The benefits bestowed by SAM may be due to its role as a methyl donor in biochemical processes governing lipid homeostasis, DNA stability, gene expression, and neurotransmitter release.

Inositol is a family of cyclic sugar alcohols consisting of nine stereoisomers of hexahydroxycyclohexane. The stereoisomers of the inositol family are myo-, scyllo-, muco-, neo-, allo-, epi-, cis-, and the enantiomers L- and D-chiro-inositol. Of these, myo-inositol and D-chiro-inositol are among the most abundant biologically active forms. The enzyme epimerase converts myo-inositol to the D-chiro-inositol isomer, maintaining organ-specific ratios of the two isomers. Physiologically, the concentration of myo-inositol is several times higher than D-chiro-inositol in most tissues.

The myo-inositol derivative phosphatidylinositol is an important component of the lipid bilayer of cell membranes. Phosphatidylinositol and its phosphorylated forms act as second messengers that are involved in a host of cellular functions including membrane trafficking, autophagy, cell migration, and survival. Disruption of phosphoinositide lipid signaling is implicated in cancer, diabetes, and cardiovascular disorders.

Inositol has shown clinical benefits in treating disorders associated with metabolic syndrome. Inositol supplementation has been effectively used to accelerate weight loss, reduce fat mass, improve serum lipid profiles and upregulate the expression of genes involved in lipid metabolism and insulin sensitivity in women with polycystic ovarian syndrome. Myo-inositol alone or in combination with D-chiro-inositol significantly reduced weight, BMI, and waist-hip circumference ratios in overweight/obese women with PCOS. Weight loss, reduction in fat mass and increase in lean mass were accelerated when inositol supplementation was accompanied by a low-calorie diet. In addition, inositol supplementation was associated with lower rate of gestational diabetes and preterm delivery in pregnant women. Currently, research is being performed to assess whether inositol may be used in treating various cancers.


Choline is an essential nutrient required for optimal functioning of various tissues including the liver, muscles, and brain. Since choline breaks down fat as an energy source, choline supplementation caused rapid fat and weight loss in female athletes. Only small amounts of choline are synthesized by the human body, necessitating its intake from external sources. In the body, about 95% of the total choline pool is converted to phosphatidylcholine – an essential component of the phospholipid bilayer and the predominant phospholipid in most mammalian cells. Choline also undergoes acetylation to form the neurotransmitter acetylcholine. Choline deficiency causes hepatic steatosis (fatty liver disease) and leads to loss of muscle membrane integrity. Chronic choline deficiency may also increase the risk of developing cancer.

Both choline and methionine are a source of methyl groups for the one-carbon transmethylation pathway and serve hepato-protective functions. Culturing hepatocytes in choline and methionine-deficient media impaired VLDL secretion. In addition, choline can donate methyl groups to support methionine regeneration, possibly contributing to their synergistic lipotropic effects.

An essential sulfur-containing amino acid, methionine undergoes transmethylation reactions to generate metabolic by-products including S-adenosyl methionine (SAM) and homocysteine. SAM is a universal methyl group donor that serves as a co-factor in numerous cellular and physiological processes including lipid homeostasis. By donating its methyl group, SAM is converted first to S-adenosyl homocysteine (SAH) and then to homocysteine. As a methyl donor, SAM contributes to the formation of phosphatidylethanolamine and subsequently to phosphatidylcholine. In the liver, phosphatidylcholine is packaged into very low-density lipoproteins (VLDL) and transported to other tissues. Inadequate levels of SAM in the liver disrupts VLDL assembly and leads to hepatic accumulation of triglycerides or fatty liver.

By promoting DNA methylation SAM plays a crucial role in epigenetic regulation. Methylation near gene promoters is a well-known mechanism of transcriptional repression. Therefore, SAM may act as a sensor for cellular nutrient status and epigenetically alter the expression of genes influencing appetite, glucose metabolism, and lipogenesis. SAM also functions as a methyl donor in the synthesis of creatine – a high-energy molecule known to improve exercise.


Structurally, all inositol stereoisomers are 6-carbon sugar alcohols with the same molecular formula as glucose (C6H12O6). Myo-inositol and D-chiro-inositol have insulin-mimetic effects. Inositol administration in diabetic rodents, rhesus monkeys, and humans lowers post-prandial blood glucose levels and improves insulin sensitivity. These benefits may be attributed to the effects of inositol on the insulin signaling pathway. Stimulating the insulin receptor activates the phosphatidylinositol-3-kinase (PI3K) pathway. Phosphorylated forms of phosphatidylinositol act as second messengers that lead to downstream activation of Akt. Akt inactivates the enzyme glycogen synthase kinase-3, enhancing glycogen synthase activity. This increases translocation of the glucose transporter (GLUT4) to the surface of skeletal muscle cells, increasing glucose uptake and lowering blood glucose levels.

Excess circulating glucose is often deposited as fat in the liver and around visceral organs. Dietary supplementation with inositol reduced weight gain and lipid accumulation in the liver of rats. Inositol-mediated activation of PI3K/Akt signaling is believed to play a role in hepatic lipid metabolism and gluconeogenesis. Inositol also affects transcription of SREBP-1 and PPAR-α – genes involved in fatty acid synthesis, oxidation, and lipid transport.


In its unmodified form, or after oxidation to betaine, choline reduces fat deposition and accelerates the lipid transport. Like methionine, betaine can also methylate DNA and influence gene expression. Consequently, choline and betaine methylated the promoter region of PPAR-α, suppressing mRNA expression and possibly the lipogenic actions of the encoded protein. In addition, choline inhibited obesity-induced oxidative stress and prevented hepatic accumulation of triglycerides.

In female athletes, choline supplementation significantly reduced body fat as well as levels of the hunger hormone leptin. Reduction in leptin levels are linked to greater food satiety. Thus, the dual advantage of consuming fewer calories while burning fats as an energy source may contribute to the lipotropic actions of choline.
Clinical Pharmacokinetics
Methionine is primarily metabolized in the liver. It is transported into hepatocytes via facilitative transport. Methionine metabolism consists of three parts: the methionine cycle, the transsulfuration pathway, and the salvage cycle. In the first step of the methionine cycle, the enzyme methyl adenosyltransferase catalyzes the conversion of methionine to S-adenosyl methionine (SAM). SAM donates its methyl group, generating S-adenosyl homocysteine, which is then hydrolyzed to adenosine and homocysteine. Homocysteine may be remethylated to regenerate methionine. Alternatively, it can be converted to cysteine via the transsulfuration pathway. In the salvage pathway, SAM is decarboxylated and used as an aminopropyl donor for polyamine biosynthesis. In healthy human subjects, 9-15% of methionine was excreted through urine following oral ingestion of 1-1.5 g of methionine. Decrease in urinary excretion occurred when the subjects were on a high-fat diet.
Myo-inositol and inositol phosphate derivatives are primarily absorbed in the gut. Cellular uptake of inositol occurs via sodium ion-coupled transporters as well as sodium-glucose co-transporters. Because they compete for the same transporters for uptake into cells, high glucose levels can significantly inhibit the uptake of inositol. Kidneys are the main sites for breakdown of inositol. Renal cortical tubules express the enzyme myo-inositol oxygenase. This enzyme metabolizes myo-inositol via the glucuronate-xylulose pathway, converting it into the monosaccharides xylulose and ribulose. Inositol that is unmetabolized or not re-absorbed at the renal tubular level is excreted unchanged through urine. Although most studies have evaluated the pharmacokinetics of inositol following oral administration, one study assessed the pharmacokinetics of myo-inositol following intravenous (IV) administration in preterm infants. In this study, the serum half-life of inositol following a single IV dose was 5.22 hours and after multiple IV dosing was 7.9 hours.
Choline obtained through the diet is absorbed by choline transporters in the intestine. Choline is primarily metabolized in the liver. Here, choline is converted to phosphatidylcholine via the cytidine diphosphate (CDP)-choline pathway. It may also be converted to betaine in a two-step irreversible reaction. Betaine contributes methyl groups to the one-carbon pathway, resulting in the regeneration of methionine from homocysteine. The metabolism of choline may be impaired by single nucleotide polymorphisms in genes encoding folate metabolizing enzymes. Furthermore, dietary choline is converted to trimethylamine by gut bacteria. Trimethylamine is oxidized to trimethylamine-N-oxide by flavin monooxygenase 3 (FMO3) in the liver. Trimethylamine-N-oxide is then excreted through urine. Impaired expression or function of FMO3 enzyme manifests as trimethylaminuria or Fish Odor Syndrome.
Pregnancy / Breast-Feeding
There are no randomized, controlled trials studying the effect of Lipo-MIC injections on pregnant and lactating women or their offspring. Human and animal studies on each constituent compound may offer some insights.
Excess methionine in the maternal diet may be detrimental to fetal development. This is because additional glycine and serine may be required to catabolize the excess methionine, inadvertently resulting in the deficiency of these amino acids. Excess methionine may also be metabolized to homocysteine. Elevated plasma homocysteine levels are associated with preeclampsia, spontaneous abortion, placental rupture, and miscarriage.
Given its use in the treatment of polycystic ovarian syndrome and gestational diabetes, myo-inositol may be considered relatively safe during pregnancy. In a meta-analysis of randomized controlled trials, 2 g of myo-inositol administered orally twice daily was reported to be safe during pregnancy. However, high concentrations of D-chiro-inositol negatively affect the quality of oocytes. Therefore, D-chiro-inositol may not be used by women seeking to get pregnant. Effects of other inositol isomers are not well characterized.
Choline requirements are especially high in pregnant women and nursing mothers. In women of reproductive age, 425 mg/day of choline is considered adequate. Adequate choline intake increases to 450 mg/day during pregnancy and 550 mg/day in lactating women. Choline supplementation had beneficial effects on fetal neurodevelopment and maternal placental function. Randomized controlled studies have reported up to 900 mg/day of choline administered orally to be safe and free of adverse events in healthy pregnant women. However, too low and excessively high levels of choline may adversely affect fetal health and development. Additionally, consuming more than 3.5 g/d of choline may cause fishy odor and hypotension in adults.
Women who are pregnant, planning to be pregnant, or are breastfeeding must consult their physician regarding the use of lipotropic injections for weight loss.
Drug Interactions
The methionine metabolite S-adenosyl methionine (SAM) may interact with antidepressants, antipsychotics, amphetamines, and narcotics causing excess accumulation of serotonin in the body. It may also interact with the cough suppressant dextromethorphan and the dietary supplement St. John’s wort, leading to increased risk of serotonin syndrome. Mild symptoms of serotonin syndrome include shivering and diarrhea, while severe symptoms include muscle rigidity, fever, and seizures.
Choline and inositol are not known to have any clinically relevant interactions with drugs, supplements, or foods.
Side Effects of Lipo (MIC) Injection
Potential side effects of lipotropic injections include:

  • Pain or soreness at the site of injection
  • Diarrhea
  • Constipation
  • Anxiety
  • Increased heart rate
  • Incontinence
  • Insomnia
  • Dry mouth
  • Fatigue
  • Numbness of hands and feet

  • This is not a comprehensive list of adverse effects. If you experience rash, hives, itchiness, shortness of breath, or other symptoms of an allergic reaction, please discontinue use immediately and consult your physician. Side effects may vary from person to person.

Safety Measures
Upcoming evidence indicates that the choline metabolite trimethylamine-N-oxide may be a risk factor for cardiovascular diseases. Studies in animal models suggest that TMAO may be atherogenic and prothrombotic. Therefore, Lipo-MIC injections are contraindicated in individuals with cardiovascular disorders. S-adenosyl methionine may worsen the symptoms of mania in people with bipolar disorder. Consult a physician before use.
How To Store
Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain
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