Combating Obesity

Rhesus monkeys and mice treated with the peptidomimetic chemical Adipotide lost significant weight. CKGGRAKDC-GG-D(KLAKLAK) is its nucleotide sequence. Research indicates that it works by causing selective apoptosis in the blood arteries that feed white adipose tissue. Adipotide promotes atrophy (shrinkage) and then apoptosis (cell death) of these arteries, which prevents them from delivering blood to the fat cells. Ischemic damage, caused by a lack of oxygen and blood flow to the fat cells, is the outcome. As a result of the irreversible impacts, fat cells also die off via apoptosis.

FTPP Adipotide‘s stereochemical structure allows it to bind to two receptors that are only present in the blood arteries that feed white adipose tissue, as proven by molecular research. Prevention and ANXA-2 are examples of such receptors. Adipotide does not influence adaptive brown fat thermogenesis since its effects are tissue-specific. With their large surface area to volume ratio, young infants lose heat disproportionately fast, making brown fat thermogenesis all the more critical. Only when calorie intake surpasses calorie expenditure can white fatty tissue develop.


Epidemiological research conducted in 2008 revealed that obesity affects 33.9% of the adult population in the United States. Excess fatty tissue bulk leads to obesity. Scientific studies have identified white adipose tissue as the primary contributor to obesity. Body weight gain is not always indicative of obesity since it may result from an increase in lean body mass rather than fatty tissue. Incidences of illness and death both rise in tandem with obesity. Anthropometry (by measuring skinfold thickness) and densitometry (using x-rays) are the current gold standards for measuring obesity. When a subject’s body mass index (BMI) reaches 30, they are considered obese. Adiposity increases a subject’s risk for several diseases and conditions. These include high blood pressure, high cholesterol, metabolic syndrome, type 2 diabetes (non-insulin-dependent), stroke, heart attack, and cancer. In particular, abdominal obesity is associated with a higher risk of morbidity than adiposity confined to the buttocks and lower extremities. Because of its usefulness in clinical settings, the waist-to-hip ratio has become a standard measure of risk for the conditions mentioned above. Intra-abdominal adipocytes are more politically active than adipocytes in the lower extremities, which may explain the correlation between abdominal obesity and more significant morbidity.

Adipocytes and the vascular/stromal compartment, in which macrophages and preadipocytes are found, make up fatty tissue. An increase in adipose mass is the outcome of the hypertrophy and subsequent hyperplasia of fatty cells brought on by an increase in lipid accumulation. The development of preadipocytes into adipocytes and the quantity of infiltrating macrophages rise throughout this process. Adipose tissue requires a constant blood supply to allow for differentiation and maintain an increasing adipose mass. Adipose cells damaged by ischemia would be unable to differentiate and instead undergo apoptotic cell death. Adipotide and other peptidomimetic substances work by inflicting irreversible ischemia damage on white adipose tissue adipocytes, decreasing the number of these cells and, hence, total adipose tissue mass. The following research provides evidence for this conclusion:

Selective Studies in Research

One such research, “Reversal of obesity by targeted ablation of adipose tissue,” was undertaken in 2004. The research presented here has been published in the scholarly journal Nature Medicine. This research aimed to prove that anti-obesity treatment based on the targeted stimulation of vascular apoptosis in the vascular base of white adipose tissue is feasible. Mice were used in the experiment. A peptide motif (CKGGRAKDC) was isolated for its ability to target blood vessels in white adipose tissue specifically. The peptide motif was found using in vivo phage display. In this work, the peptide motif interacted with prohibitin, a multifunctional membrane protein. This proved that prohibitin marked blood vessels in white adipose tissue. The results also showed that the adipose tissue mass might be eliminated by pro-apoptotic peptide targeting the white adipose tissue vasculature. Normalization of the metabolic processes as a natural result of the white fat resorption. There were no severe side effects associated with this normalization. Since humans express prohibitin in their white adipose tissue vasculature, it might be deduced that the same peptide pattern would eliminate white fat mass in subjects. 


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