Fragment 176-191 Peptide | Ultimate Guide

One of the unique properties of Fragment 176-191 is its ability to specifically target and stimulate the breakdown of adipose (fat) tissue. It is believed to work by increasing lipolysis, which is the process of breaking down stored fat into fatty acids for energy utilization. Fragment 176-191 has been shown to have a higher affinity for fat cells compared to other tissues, making it a potential candidate for promoting fat loss without significant effects on other body tissues.You can learn more about this peptide by visiting Peptide Sciences.

Research studies, mainly conducted on animal models and in vitro experiments, have shown promising results regarding the ability of Fragment 176-191 to reduce body fat and promote weight loss. However, it's important to note that more research is needed to fully understand its potential benefits and risks in weight loss.

Additional research that Fragment 176-191 cost may make it a useful adjuvant in chemotherapy given that the peptide can boost the effects of existing medications for cancer treatment while simultaneously reducing side effects. It has also been investigated for its ability to improve cartilage health in the setting of osteoarthritis.

Fragment 176-191 Structure

Sequence: Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe-Tyr
Molecular Formula: C78H123N23O22S2?
Molecular Weight: 1799.1 g/mol
PubChem CID: 16131230
Cas No.: 66004-57-7
Synonyms: GH (176-191), Somatotropin (176-191)

Source: PubChem
URL: https://pubchem.ncbi.nlm.nih.gov/compound/16131230
Data deposited in or computed by PubChem

What Is Fragment 176-191?

The best way to respond to the question of what Fragment 176-191 is to state, simply, that it is part (a fragment) of the hormone that causes a natural growth hormone release. Getting more specific requires an understanding of what a growth hormone-releasing hormone (GHRH) analogue is and why Fragment 176-191 is slightly different from peptides like Sermorelin and CJC-1295.

A growth hormone-releasing hormone analogue is a synthetic compound that mimics the action of naturally occurring GHRH in the body. GHRH is a hormone produced in the hypothalamus that stimulates the natural release of growth hormone (GH) from the pituitary gland. GH plays a crucial role in various physiological processes, including growth, metabolism, and body composition.

GHRH analogues are designed to enhance a natural GH release and can be used for diagnostic or therapeutic purposes. Sermorelin, for instance, is typically used in the diagnosis of growth hormone deficiency (GHD). Additionally, GHRH analogues have been investigated for their potential therapeutic applications in conditions such as age-related muscle loss, wasting disorders, and certain hormonal deficiencies.

Most GHRH analogues consist of a slightly modified form of natural GHRH. CJC-1295, for instance, has a handful of amino acid substitutions that give it a longer half-life and better storage characteristics than standard GHRH. Fragment 176-191 is different, however. It is only a small portion of the larger GHRH.

Researchers learned, after studying a variety of synthetic derivatives of GHRH, that certain parts of the peptide have different activity. The portion corresponding to amino acids numbered 176 to 191, turns out to retain most of the parent molecule’s fat-burning properties and very few of the parent molecule's other activity, such as increased bone and muscle growth. Now, it may seem undesirable to remove such effects as they clearly have benefits, but having a highly targeted fat burning peptide is also of benefit. Its impressive and highly specific fat burning properties are what led to Fragment 176-191 becoming known as the “lipolytic fragment.”

As a somewhat tangential but still important aside, Fragment 176-191 and AOD9604 are sometimes used interchangeably. This is understandable given the extreme similarities both in the structure and function of these peptides. AOD9604 is just one amino acid shorter than Fragment 176-191, being made up of amino acids 177-191 of HGH. Much of the research into Fragment 176-191 applies to AOD9604 and vice versa, but the two peptides are slightly different. These differences may be critical to certain research projects and not so important to others. Pay careful attention to the length of the peptide being purchased to avoid confusion as not only are the peptides similar in structure and function but Fragment 176-191 cost is basically identical to AOD9604 cost.

Fragment 176-191: The Lipolytic Fragment

Studies in mice have shown that Fragment 176-191 exhibits lipolytic properties, meaning it can promote the breakdown of fat cells and enhance fat burning[1]. It is believed that this effect is mediated through the increased production of beta-3 adrenergic receptors (β3-AR or ADRB3). Activation of ADRB3 receptors in adipose tissue can stimulate lipolysis, the release of stored fatty acids for energy utilization[2].

The lipolytic effects of Fragment 176-191 appear to be independent of the growth-promoting effects of the full-length HGH molecule. In mice lacking ADRB3 receptors, the response to HGH or Fragment 176-191 is diminished, suggesting that ADRB3 receptors play a role in mediating the lipolytic effects. However, it is also suggested that there may be additional mechanisms involved that are not yet fully understood.

What is interesting is that research reveals that HGH and its C-terminal fragment reduce body weight gain, increase fat oxidation, and stimulate lipolysis in obese mice, without interacting with the HGH receptor[3]. This research confirms a concept, which has long been held in science, that HGH is both a hormone and prohormone. This means that while HGH binds to GH receptors as an intact molecule to cause certain effects, it can also be broken down into different pieces and some or all those pieces can have additional effects that are not necessarily shared with the larger HGH peptide or with one another. Fragment 176-191 is the peptide that made this hypothesis fully concrete and helped to open new avenues of research not just for HGH, but for a variety of peptide hormones.

Fragment 176-191 for Fat Burning

The above paragraphs explain why Fragment 176-191 is called the lipolytic fragment, but they don’t indicate how effective it is. Research in rat models suggests that daily use of Fragment 176-191 can lead to a reduction in weight gain of 50%. In other words, the two populations of rats gained weight because they were already obese, and they were allowed to eat whatever they wanted. The rats given Fragment 176-191, however, gained only half as much weight as the untreated rats[4].

What is really intriguing about the rats treated with Fragment 176-191 is that they did not develop insulin resistance. Insulin resistance is a well-documented side effect of long-term treatment with growth hormones. In fact, insulin resistance is one of the major reasons that treatment with HGH is generally avoided in favor of peptides, like sermorelin, that stimulate HGH release indirectly. The fact that Fragment 176-191 boosts fat burning without affecting insulin makes it an excellent candidate for development into an orally usable and safe therapeutic for weight loss. This fact alone reinforces why, sometimes, it is better to have a highly targeted peptide rather than one with wide-ranging effects.

Further study of the rats revealed that Fragment 176-191 stimulated hormone-sensitive lipase and inhibited acetyl coenzyme A carboxylase in fat cells. This means that the peptide increased the production of the enzyme that breaks down fat and inhibited the enzyme that creates fat. The mice showed fat cells that were, on average, only 72% as large as those in untreated rats[5], [6].

Another study investigated the effect of Fragment 176-191 on glucose transport in adipocytes isolated from genetically obese Zucker rats. The results indicated that the synthetic peptide caused a decrease in both basal and insulin-stimulated uptake of D[1-14C]-2-deoxyglucose in the isolated adipocytes. In other words, Fragment 176-191 interferes with the uptake of glucose by fat cells. This means that more glucose is available for other tasks, such as muscle glycogen storage, and that fat cells are deprived of the raw materials they need to grow.

The study also found that Fragment 176-191 is more potent, even at the same concentrations, as the intact human growth hormone (HGH). This further supports the idea that the C-terminal region of the HGH molecule, which includes Fragment 176-191, is responsible for the anti-lipogenic activity of HGH[7].

Everything discussed above is in keeping with another fact that has been well-understood since the mid-1980s. The amino-terminal (n-terminal) end of HGH contains a short sequence of peptides (positions 6-13) that enhance the transport of glucose into adipose tissue via the 3-O-methylglucose transporter. This fact explains why intact HGH is not as effective as Fragment 176-191 alone at reducing lipogenesis. It would seem that intact HGH actually has some competing properties and that the c-terminal end is responsible for fat burning and probably is more potent than the fat-promoting n-terminal end[8], [9]. The point, an isolated fragment of HGH can and does have important properties of its own.

Fragment 176-191 and Diabetes

As noted above, Fragment 176-191 has an interesting impact on the effects of insulin. For fat cells, it appears that Fragment 176-191 prevents the uptake of glucose, and this is how it helps to burn fat. Research also shows, however, that the C-terminal end of human growth hormone (HGH) plays a crucial role in its hypoglycemic effects, which refers to its ability to lower blood sugar levels. Several experiments involving the testing of various fragments derived from this section of HGH have revealed that Fragment 176-191 is particularly effective in increasing blood glucose levels.

Fragment 176-191 has been identified as the most potent synthetic derivative of HGH for increasing blood sugar [10]. This may sound precisely the opposite of what you would want in diabetes, particularly because the increase in blood sugar occurs in conjunction with an increase in insulin resistance.

The insulin resistance that occurs through administration of Fragment 176-191 is different from the insulin resistance that occurs in the setting of diabetes. In diabetes, more and more insulin is needed to get the same amount of glucose into cells of all types. In other words, insulin resistance in diabetes results when muscle, fat, and liver become more immune to the effects of insulin. The result is that blood sugar rises, and the pancreas responds by producing more insulin. This vicious cycle eventually results in burnout of the pancreas as well as consistently elevated blood sugar levels that lead to all kinds of problems.

The insulin resistance of Fragment 176-191 appears to only affect fat cells. Both liver and muscle remain sensitive to insulin and continue to take up glucose. Interestingly, research indicates that the primary defect in type 2 diabetes is a failure of skeletal muscle to take up glucose secondary to insulin resistance. With Fragment 176-191, it is adipose tissue that is made insulin resistant while skeletal muscle remains insulin sensitive[11]. In fact, upwards of 90% of plasma glucose is taken up by muscle in response to insulin. This means that even though Fragment 176-191 does cause insulin resistance, it is not the insulin resistance of diabetes. The result is that the excess glucose is taken up by muscle and thus fat mass decreases. This is another point where the insulin resistance of diabetes and Fragment 176-191 differ. With diabetes, the muscle is basically impervious to insulin and the glucose has nowhere to go but into fat. Increasing adipose tissue leads to inflammation that may be a driver of much of the vascular damage seen in diabetes. With the insulin resistance of Fragment 176-191, muscle continues to take up glucose at an ever-increasing rate and does not contribute to inflammation.

Overview of how adipose tissue contributes to inflammation.
Source: Creative Diagnostics
URL: https://www.creative-diagnostics.com/adipocytokine-signaling-pathway.htm

Over time, a decrease in adipose tissue will improve insulin resistance by driving down inflammation. Research shows that inflammatory cytokines like tumor necrosis factor alpha are major contributors to insulin resistance. Adipose tissue is specifically designed to store large amounts of fat, and its fat cells, known as adipocytes, can accommodate significant quantities of triglycerides, the primary form of stored fat. The adipose tissue is characterized by its abundance of stem cells, which can differentiate into new fat cells when needed to accommodate excess energy such as triglycerides. This capacity to generate new fat cells allows the adipose tissue to expand and store additional fat as required.

As long as the fat cells within the adipose tissue remain healthy, there are typically no adverse metabolic effects, aside from the obvious consequence of excess weight. In fact, about one-third of individuals classified as obese fall into a category referred to as "metabolically healthy obese." These individuals have excess body fat but do not exhibit the metabolic disturbances typically associated with insulin resistance. However, while the adipose tissue can expand and store excess fat, capacity is not unlimited. When fat cells become over-expanded due to excessive calorie intake and weight gain, several negative consequences can occur.

One of these consequences is the development of hypoxia, which refers to a reduced oxygen supply to the adipose tissue due to inadequate blood flow. Hypoxia activates the HIF-1 gene, leading to increased expression of proteins called JNK and IKK that contribute to the initiation of inflammation within the fat cells. The inflammation within the fat cells then leads to insulin resistance. Insulin normally acts as an anti-lipolytic hormone in the adipose tissue, suppressing the release of stored fatty acids by inhibiting the activity of hormone-sensitive lipase (HSL). However, with the development of inflammation and insulin resistance in fat cells, there is increased lipolysis, causing higher levels of free fatty acids (FFA) to be released into the bloodstream.

The released fatty acids can be taken up by other organs, such as the liver and skeletal muscles, which are not designed to store large amounts of fat. This can lead to the development of insulin resistance in these organs as well. Furthermore, the increased inflammation in the fat cells attracts a greater number of M1 macrophages, a pro-inflammatory type of immune cell. These macrophages release inflammatory cytokines, including TNFα, which further contributes to insulin resistance and lipolysis.

In lean individuals, only a small portion of the adipose tissue mass is composed of macrophages, primarily in the anti-inflammatory M2 state. However, in obese individuals, a larger proportion of the adipose tissue may contain macrophages, predominantly in the pro-inflammatory M1 state.

The presence of inflammation, insulin resistance, and an imbalance of M1 macrophages in the adipose tissue contributes to the dysregulation of lipid metabolism, promoting further weight gain and the development of metabolic disorders associated with obesity[12]. In the end, this is why insulin resistance caused by Fragment 176-191 is different from the insulin resistance seen in diabetes. For Fragment 176-191, it augments and does not detract from glucose uptake in muscle and liver while interfering with the same process in fat cells. While the early consequence is increased insulin resistance, the problem slowly resolves itself as fat is eliminated.

Fragment 176-191 and Musculoskeletal Function

In all of the discussions about Fragment 176-191 in regard to fat loss and insulin resistance, it can be easy to forget that this small peptide is part of the larger GH molecule. GH hormone has properties that go well beyond burning fat, so does Fragment 176-191 also have additional properties? Given its relatively small size compared to GH and its exceptionally potent fat-burning capabilities, it would be reasonable to conclude that Fragment 176-191 is highly specialized in its function. As it turns out, however, Fragment 176-191 has a multitude of other properties. Then the next several sections explore these additional features of Fragment 176-191, with this section focusing on its role in the musculoskeletal system.

In a study using a rabbit model of collagenase-induced osteoarthritis, the researchers investigated the additional effects of intra-articular administration of recombinant human growth hormone (GH) in combination with hyaluronic acid (HA). The experiment involved mature New Zealand white rabbits divided into three groups.

Group 1 (control) received weekly intra-articular saline injections for four weeks. Group 2 received 6 mg of HA injections, and group 3 received 6 mg of HA combined with 3 mg of recombinant human GH. These injections were initiated four weeks after collagenase injections. Lameness was observed for a total of nine weeks following collagenase injections, and at the end of this period, macroscopic and histopathological evaluations of the knee joint were conducted.

Although all animals exhibited lameness after collagenase injections, the duration and severity of lameness were significantly reduced in group 3 compared to groups 1 and 2. Macroscopic evaluations indicated that the femoral condyles of rabbits in group 3 had significantly less cartilage damage compared to those in groups 1 and 2. Histopathological scores were also the lowest in group 3 (P<0.01).

These findings suggest that the co-injection of intra-articular HA and recombinant human GH is more effective in mitigating the symptoms of osteoarthritis compared to HA injections alone, as observed in this osteoarthritis model using rabbits. It indicates a potential additive effect of recombinant human GH in combination with HA, leading to reduced lameness and cartilage damage in the knee joint[13].

Similar research with Fragment 176-191 shows that it too has beneficial effects on cartilage repair and healing. In another study using a collagenase-induced knee osteoarthritis (OA) rabbit model, researchers investigated the effects of intra-articular injections of Fragment 176-191, a synthetic peptide fragment derived from human growth hormone, with or without hyaluronic acid (HA) and ultrasound guidance.

The study found that intra-articular Fragment 176-191 injections, guided by ultrasound, promoted cartilage regeneration in the knee joint. Moreover, the combination of Fragment 176-191 and HA injections was more effective in enhancing cartilage regeneration compared to either Fragment 176-191 or HA injections alone.

The specific mechanisms by which Fragment 176-191 promotes cartilage regeneration are not clear, but it is worth noting that Fragment 176-191 has been previously studied for its potential to enhance cartilage repair and protect against cartilage degradation. It is believed to have anti-inflammatory and chondroprotective properties, making it a promising candidate for the treatment of OA[14].

Keep in mind that research suggests that HGH, and by extension Fragment 176-191, have several effects in cartilage that can impact healing and recovery. Research in cell cultures shows that these peptides can double cell counts for repair cells like fibroblasts and boost matrix deposition. This latter feature is probably a result of the 2x increase in fibroblasts, the cells responsible for producing cartilage and extracellular matrix. Fibroblasts are known to have HGH receptors, which is most likely why they are affected by HGH. What about chondrocytes though, the cells responsible for building cartilage?

Chondrocytes are specialized cells found in cartilage tissue. They are responsible for the synthesis and maintenance of the extracellular matrix of cartilage, which provides structure, elasticity, and mechanical support to the tissue. Chondrocytes produce various components of the extracellular matrix, including collagen, proteoglycans, and other matrix proteins.

Chondrocytes play a crucial role in the growth, development, and repair of cartilage. During development, chondrocytes contribute to the formation of the skeletal system by producing cartilage models that later undergo ossification. In adult cartilage, chondrocytes help maintain the integrity and homeostasis of the tissue by balancing the synthesis and degradation of the extracellular matrix components.

Chondrocytes are embedded within the extracellular matrix of cartilage and are housed within small spaces called lacunae. These cells have a rounded or ovoid shape and possess a characteristic feature called the chondrocyte lacunar-canalicular system. This system consists of interconnected channels that allow communication between chondrocytes and facilitate the exchange of nutrients, waste products, and signaling molecules within the cartilage tissue.

In response to mechanical stress, injury, or pathological conditions, chondrocytes can undergo changes in their activity and behavior. They can proliferate, differentiate, and produce factors involved in cartilage repair and regeneration. However, in conditions such as osteoarthritis, the function of chondrocytes can be impaired, leading to cartilage degradation and loss. Research in rabbits suggests that HGH promotes mitosis among chondrocytes[15]. It is likely that Fragment 176-191 does the same.

The role of the growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis in OA is still not completely understood and remains an area of ongoing research. Studies have suggested that there may be a complex relationship between GH/IGF-1 signaling and the development and progression of OA.

One finding that has emerged is the existence of a bell-shaped relationship between GH/IGF-1 signals and OA. This means that both too-low and too-high levels of these hormones may be associated with an increased risk or severity of joint disease.

Low levels of GH/IGF-1 may have a detrimental effect on cartilage maintenance and repair processes, potentially contributing to the development of OA. On the other hand, excessively high levels of GH/IGF-1 may also be problematic and could promote abnormal bone and cartilage growth, leading to joint deformities and osteophyte formation.

The exact mechanisms by which GH/IGF-1 axis influences OA pathogenesis are still being elucidated. It is believed that these hormones play a role in regulating cartilage metabolism, chondrocyte function, and the balance between anabolic and catabolic processes in the joint. Changes in GH/IGF-1 levels or their signaling pathways can disrupt this balance and contribute to cartilage degradation and the?
development of OA[16].

?
Illustration of the bell curve reflecting that both too little and too much GH can lead to osteoarthritis.
Source: National Library of Medicine
URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7736189/

Fragment 176-191 and Cancer

Many drugs used to treat cancer can have limitations in terms of tumor targeting and their impact on healthy tissues. The goal of cancer treatment is to effectively target and destroy cancer cells while minimizing damage to normal cells and tissues.

In recent years, there have been advancements in the development of targeted therapies that aim to specifically target cancer cells while sparing healthy cells. These therapies are designed to exploit unique characteristics or vulnerabilities of cancer cells, such as specific genetic mutations or overexpressed proteins.

Examples of targeted therapies include monoclonal antibodies, which are designed to bind to specific proteins on cancer cells, and small molecule inhibitors that block specific signaling pathways involved in cancer growth and survival. These approaches can enhance the specificity and effectiveness of treatment while minimizing toxicity to normal tissues.

Additionally, there are ongoing efforts to improve drug delivery systems and develop strategies for more precise tumor targeting. This includes the use of nanoparticles, liposomes, and other drug carriers that can deliver therapeutic agents directly to tumor sites, increasing their concentration in cancer cells while reducing exposure to healthy tissues.

Fragment 176-191 turns out to work synergistically with some chemotherapeutic agents to increase the anti-proliferative properties of the drugs against certain types of tumors. What is even more compelling is that the use of Fragment 176-191 in this way helps to reduce the clinical side effects associated with off-target exposure to chemotherapy[17].

Fragment 176-191 Cost

Fragment 176-191 cost has been mentioned several times as a positive. Peptides are relatively easy to produce in large quantities and of high quality. These features make them very cost effective for research purposes and as therapeutics. With the rising cost of everything from over-the-counter medications to prescription drugs, it is refreshing to see research being carried out on peptides that may one day provide affordable treatment options for several diseases.

The cost of Fragment 176-191 can vary depending on several factors, including the supplier, the purity and quality of the product, the quantity purchased, and the region or country of purchase. A trusted supplier is always worth the extra money so that contaminants or incorrect products do not taint research results.

Fragment 176-191 Overview

So, what is Fragment 176-191 in summary? Fragment 176-191 is a synthetic component of the c-terminal end of human growth hormone known mostly for its fat-burning properties. Fragment 176-191 is more than just a fat-burning peptide though. Research has indicated that it might be useful in the treatment of diabetes, as an adjuvant to chemotherapy, and as a potential treatment for osteoarthritis. Fragment 176-191 cost is low making it a very promising peptide for research projects aimed at further unraveling the multitude of functions of various fragments of HGH. With the recent resurgence of interest in peptides that help to burn fat, it would not be surprising at all if Fragment 176-191 experiences a research renaissance soon.

Resources

[1]?? ?M. Heffernan et al., “The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and beta(3)-AR knock-out mice,” Endocrinology, vol. 142, no. 12, Art. no. 12, Dec. 2001, doi: 10.1210/endo.142.12.8522.
[2]?? ?R. Ferrer-Lorente, C. Cabot, J.-A. Fernández-López, and M. Alemany, “Combined effects of oleoyl-estrone and a beta3-adrenergic agonist (CL316,243) on lipid stores of diet-induced overweight male Wistar rats,” Life Sci., vol. 77, no. 16, pp. 2051–2058, Sep. 2005, doi: 10.1016/j.lfs.2005.04.008.
[3]?? ?M. A. Heffernan et al., “Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment,” Int. J. Obes. Relat. Metab. Disord. J. Int. Assoc. Study Obes., vol. 25, no. 10, pp. 1442–1449, Oct. 2001, doi: 10.1038/sj.ijo.0801740.
[4]?? ?F. M. Ng, J. Sun, L. Sharma, R. Libinaka, W. J. Jiang, and R. Gianello, “Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone,” Horm. Res., vol. 53, no. 6, pp. 274–278, 2000, doi: 10.1159/000053183.
[5]?? ?F. M. Ng, W. J. Jiang, R. Gianello, S. Pitt, and P. Roupas, “Molecular and cellular actions of a structural domain of human growth hormone (AOD9401) on lipid metabolism in Zucker fatty rats,” J. Mol. Endocrinol., vol. 25, no. 3, pp. 287–298, Dec. 2000, doi: 10.1677/jme.0.0250287.
[6]?? ?M. A. Heffernan, W. J. Jiang, A. W. Thorburn, and F. M. Ng, “Effects of oral administration of a synthetic fragment of human growth hormone on lipid metabolism,” Am. J. Physiol. Endocrinol. Metab., vol. 279, no. 3, pp. E501-507, Sep. 2000, doi: 10.1152/ajpendo.2000.279.3.E501.
[7]?? ?E. Wijaya and F. M. Ng, “Effect of an antilipogenic fragment of human growth hormone on glucose transport in rat adipocytes,” Biochem. Mol. Biol. Int., vol. 31, no. 3, pp. 543–552, Nov. 1993.
[8]?? ?F. M. Ng and R. I. Hoich, “Stimulation of 3-O-methylglucose transport in adipocytes by a synthetic human growth hormone fragment,” Biochem. Int., vol. 10, no. 3, pp. 507–516, Mar. 1985.
[9]?? ?L. G. Frigeri, C. Teguh, N. Ling, G. L. Wolff, and U. J. Lewis, “Increased sensitivity of adipose tissue to insulin after in vivo treatment of yellow Avy/A obese mice with amino-terminal peptides of human growth hormone,” Endocrinology, vol. 122, no. 6, pp. 2940–2945, Jun. 1988, doi: 10.1210/endo-122-6-2940.
[10]?? ?F. M. Ng and J. Bornstein, “Hyperglycemic action of synthetic C-terminal fragments of human growth hormone,” Am. J. Physiol., vol. 234, no. 5, pp. E521-526, May 1978, doi: 10.1152/ajpendo.1978.234.5.E521.
[11]?? ?R. A. DeFronzo and D. Tripathy, “Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes,” Diabetes Care, vol. 32, no. suppl_2, pp. S157–S163, Nov. 2009, doi: 10.2337/dc09-S302.
[12]?? ?B. Sears and M. Perry, “The role of fatty acids in insulin resistance,” Lipids Health Dis., vol. 14, p. 121, Sep. 2015, doi: 10.1186/s12944-015-0123-1.
[13]?? ?S. B. Kim et al., “Additive effects of intra-articular injection of growth hormone and hyaluronic acid in rabbit model of collagenase-induced osteoarthritis,” J. Korean Med. Sci., vol. 25, no. 5, pp. 776–780, May 2010, doi: 10.3346/jkms.2010.25.5.776.
[14]?? ?D. R. Kwon and G. Y. Park, “Effect of Intra-articular Injection of AOD9604 with or without Hyaluronic Acid in Rabbit Osteoarthritis Model,” Ann. Clin. Lab. Sci., vol. 45, no. 4, pp. 426–432, 2015.
[15]?? ?A. S. Hendricson, T. Havdrup, and H. Telhag, “The effect of growth hormone and thyroxine on adult joint cartilage,” Clin. Orthop., no. 162, pp. 270–275, 1982.
[16]?? ?M. Dixit, S. B. Poudel, and S. Yakar, “Effects of GH/IGF axis on bone and cartilage,” Mol. Cell. Endocrinol., vol. 519, p. 111052, Jan. 2021, doi: 10.1016/j.mce.2020.111052.
[17]?? ?M. M. Habibullah et al., “Human Growth Hormone Fragment 176-191 Peptide Enhances the Toxicity of Doxorubicin-Loaded Chitosan Nanoparticles Against MCF-7 Breast Cancer Cells,” Drug Des. Devel. Ther., vol. 16, pp. 1963–1974, 2022, doi: 10.2147/DDDT.S367586.

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