Weight Loss – “The Skinny Shot”
Tirzepatide is a once-weekly GIP (glucose-dependent insulinotropic polypeptide) receptor, and GLP-1 (glucagon-like peptide-1) receptor agonist, representing a new class of medicines studied for the treatment of obesity. Tirzepatide is a single peptide that triggers the body’s receptors for GIP and GLP-1, two natural incretin hormones. Cyanocobalamin will help increase energy.
GIP has decreased food intake and increased energy expenditure, resulting in weight reductions. Combined with a GLP-1 receptor agonist, it has a more significant effect on glucose and body weight effects.
- Substantial A1C reductions.
- Boosted weight loss.
- Improvements in cardiometabolic measures.
- Reduce appetite.
Nicotinamide-N-methyltransferase (NNMT), is a cytosolicenzyme with newly identified roles in cellular metabolism and energy homeostasis. Studies indicate that this enzyme slows down the process at which our bodies metabolize fat cells. Most people have a hard time losing weight. When this enzyme is elevated, they have a more challenging time trying to lose excess pounds of fat. The extra weight leads to an increase in the NNMT enzyme, leading to slower fat metabolism, leading to excess weight gain. It is a vicious cycle.
Research suggests a potent NNMT inhibitor “5-amino-1mq” significantly reduced body weight and white adipose mass, decreased adipocyte size, and lowered plasma total cholesterol levels. These results support the development of small molecule NNMT inhibitors as therapeutics to reverse diet-induced obesity and validate NNMT as a viable target to treat obesity and related metabolic conditions.
- Reduce the formation of fat cells and size.
- Reverse diet-induced obesity.
- ⬆Increase fat metabolism.
- ⬇ Decrease cholesterol levels.
AOD-9604 Anti Obesity Drug
AOD 9604 is a modified form of amino acids 176-191 of the GH polypeptide. Investigators at Monash University discovered that the fat-reducing effects of
GH appear to be controlled by a small region near one end of the GH molecule. This region, which consists of amino acids 176-191, is less than 10% of the total size of the GH molecule and appears not to affect growth or insulin resistance. It works by mimicking the way natural Growth Hormone regulates fat metabolism but without the adverse effects on blood sugar or growth that is seen with unmodified Growth Hormone. Like Growth Hormone, AOD 9604 stimulates lipolysis (the breakdown or destruction of fat) and inhibits lipogenesis (the transformation of nonfat food materials into body fat).
- Reduces body fat.
- Regulates fat metabolism.
- Stimulates Lipolysis.
- Inhibits Lipogenesis.
- Triggers fat release.
(mitochondrial open reading frame of the 12S rRNA-c)
MOTS-C is a short open reading frame (sORF) 16 amino-acid peptide. MOTS-C has endocrine- like effects on muscle metabolism, insulin sensitivity, and weight regulation. It regulates insulin sensitivity and metabolic homeostasis. Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle. MOTS-C targets the Methionine-Folate Cycle, Increases AICAR levels, and activates AMPK. A well-described role of AICAR is to activate AMPK and stimulate fatty acid oxidation and also enhance glucose uptake in the muscle.
MOTS-C has been shown to target the skeletal muscle and enhance glucose metabolism. As such, MOTS-C has implications in the regulation of obesity, diabetes, exercise, and longevity, representing an entirely novel mitochondrial signaling mechanism to regulate metabolism within and between cells.
MOTS-C assists with gene expression and cellular metabolism. It appeared to stimulate glucose utilization by increased glucose clearance. Coordinates cellular glucose, mitochondrial, and fatty acid metabolism.
MOTS-c prevents HFD-induced obesity by increasing energy expenditure, including heat production, improving glucose utilization and insulin sensitivity. Reduced fat accumulation may be a result of robust carbohydrate
usage that reduces fatty acid synthesis.
- Regulates insulin sensitivity and maintain metabolism.
- Stimulate fatty acid oxidation.
- Enhance glucose uptake and clearance into muscle.
- Stimulate glucose utilization.
- Coordinates cellular glucose, mitochondrial, and fatty acid metabolism.
- Increased energy expenditure and heat production.
- Reduction of fat accumulation.
Tesofensine is a dopamine, serotonin, and noradrenaline (triple) reuptake inhibitor originally developed to treat neurological disorders such as Parkinson’s disease (PD) and Alzheimer’s disease. Although tesofensine was not efficient in PD trials, overweight participants achieved significant weight loss. Tesofenesine was changed from development for these applications as it showed limited efficacy. It did show consistent weight loss especially in overweight or obese patients. Tesofensine, an inhibitor of presynaptic uptake of the neurotransmitters serotonin,
noradrenaline, and dopamine, acts primarily as an appetite suppressant with simultaneous effects on fat oxidation and resting energy expenditure. Clinical trial data suggests it may potentially achieve more significant reductions in weight than that seen with currently approved weight loss agents. In Phase 2 clinical studies, weight loss over six months was more effective than other available weight loss drugs. Patients lost an average of 12.8 kg on the 1 mg dose, 11.3 kg on the 0.5 mg
dose, and 6.7 kg on the 0.25 mg dose.
- Significantly affected appetite
- Reduction in expected next meal size
- Decreased desires for sweet, fatty, or salty foods
- Improvement in quality of life in Physical Function, Self Esteem, Sexual Life, Public Distress, and Work.