Resistin and Its Potential Effects on Insulin Resistance

Introduction to Adipokines: Specifically Resistin

The physiology of obesity is a complex perpetuation of countless hormonal processes. The secretion and reaction between such hormones are responsible for the regulation of different physiological functions throughout the body. Research is constantly evolving as the physiological understanding behind the disease progresses. Adipose tissue has been found to secrete numerous peptide formations; these peptides are referred to as adipokines or adipocytokines. The adipose cell; originally thought to be an energy-storing tissue, is now proven to be metabolically active having both enzymatic and hormonal functions.

These adipokines are commonly referred to as “gut hormones” in obesity research. Gut hormones are proven to have multiple effects throughout the body, both helpful and harmful. Functions such as glucose infusion, insulin sensitivity, insulin secretion, inflammatory response, appetite, and energy expenditure are all regulated through hormonal activity between the stomach and brain. The profile of adipocytokines in the gut varies as abdominal fat fluctuates. Excess visceral fat results in the secretion of hormones that inhibit a healthy metabolic process; insulin insensitivity, inflammation, and decreased energy expenditure are the by-products of some harmful cytokines.

The main purpose of this paper is to explore the physiological effects of the gut hormone Resistin. According to a study conducted at The Penn Diabetes Center, resistin was first discovered as a 12kDaa polypeptide by CM Steppan, et al. The focus of their research in 2001 aimed at exploring the mechanism which so closely correlates increased adiposity with increased insulin resistance (Steppan et al. 307).

Their discovery of a signaling molecule derived from adipocyte cells in rodents gave them further insight into this mechanism. Elevated levels of serum resistin in obese mice, as well as the fifteen-time higher rate of expression of resistin in visceral adipose compared to subcutaneous adipose elicited further research (Banerjee and Lazar 218). Expression of the hormone is associated with heightened resistance to insulin; desensitizing it and impairing glucose control. Both endogenous levels of circulating resistin in obese mice, as well as recombinant injections, correlate the hormone with decreased insulin sensitivity.

The experiment provided by Steppan et al. on normal mice, et al stated that the resistin reduced the glucose tolerance and the action of insulin. This experiment also shows that resisting one of the main hormones may be helpful in understanding why excessive adiposity results in insulin resistance as well as the anti-diabetic effect of a new class of drugs called thiazolidinediones. The main principle of thiazolidinediones’ work is based on their ability to increase adipose tissue sensitivity to insulin (Steppan et al. 307). Still, consuming thiazolidinediones drugs, rats’ blood glucose and insulin lowered that allowed to apprehend insulin, but this, in its turn, lead to gaining weight.

Thus, here is a paradox, excess weight prevents good insulin sensitivity. This paradox was one of the main encourages for continuing the research and looking for other ways of increasing insulin actions. The research provided in vivo and in vitro showed that resistin is able to improve insulin sensitivity and reduce glucose tolerance (Banerjee and Lazar 218). Banerjee et al. also proved that it is possible to regulate fasted blood glucose by means of resistin (1195). The main idea of resistin is to reduce glucose level and insulin resistance (McTernan et al. 6098).

Function, Regulation, and Physiological Effects of Resistin

Even though there is much research devoted to resistin and most of the studies point to the positive effect of this hormone, its influence is not considered till the end. On the one hand, resistin is helpful as it reduces insulin resistance, on the other hand, the hormone plays an essential role in adipocyte differentiation (Hartman 19761). But, providing the experiments of rats with diabetes and adiposity, it was concluded that resistin which is secreted from adipocytes may be helpful in reducing the tolerance of glucose activity and increasing insulin resistance. Resistin is a good helper in treating diabetes with thiazolidinediones drug.

But, it is highly important to consider the environment, as according to another research, resistin may be extremely harmful to glucose (may lead to its deregulation) and lipid metabolism as well as for insulin resistance in the case when resistin is over-expressed (Liu, et al 49). The research provided by Li shows that resistin may cause a number of other problems. Thus, some experiments showed that resistin may restrain hepatic AMPK activity. The main result from this inhibition may affect glucose metabolism and lead “to decreased glycogen storage that contributes to the development of hepatic IR” (Li 243). Therefore, there is no strict answer to whether resistin is good or bad for those who suffer from diabetes. Further research should be conducted to identify the proper effect of this hormone.

One of the main impacts of increased insulin resistance remains glucose intolerance which, in its turn, leads to sugar increase (Steppan et al. 309). Some research shows that there is a connection between insulin resistance and adipose mass. With the increase of one, another increases as well. This creates a number of problems for people who suffer from diabetes. Moreover, insulin resistance tells that a person with the problem does not get enough insulin which is aimed to block glucose uptake. The failure to reduce glucose uptake leads to numerous complications related to diabetes (Banerjee et al. 1195). Insulin resistance in combination with central obesity may lead to morbidity and mortality as well (Pravenec et al. 45209).

Considering insulin resistance and its effects on it, the AMPK-dependent mechanisms in HepG2 cells should be explored as well as AMPK-independent ones. Thus, according to the results achieved by Luo et al. “resistin induces insulin resistance in HepG2 cells at least partly in via introduction of SOCS-3 expression and reduction of Akt phosphorylation of SOCS-3 expression and reduction of Akt phosphorylation through an AMPK-independent mechanism” (Luo 60).

Dwelling upon possible effects on glucose intolerance, it may be completed that thiazolidinediones and resistin remain the main substances which can reduce glucose in the blood. Different dies may also have a positive effect on lowering glucose intolerance in the organism which suffers from diabetes. Resistin is the hormone that is aimed at lowering glucose intolerance and promoting normal organism functioning (McTernan 6105).

Resistin: A Link between Obesity and Diabetes?

It has already been proved that resistin has a close connection with both obesity and diabetes. To understand this relation better, the following questions should be considered, diabetes is a risk factor for obesity, mechanisms of increased insulin resistance, the ways how resistin may desensitize insulin receptors and what effect may be considered, and the possibility of the resistin link these diseases and possibly show causality between them.

Dwelling upon the first problem, diabetes and its risky influence on obesity it should be mentioned that the processes in the organism are closely connected. The change in the functioning of one system leads to changes in the whole body. Still, the connection between insulin resistance and obesity is unknown. But, it is easy to prove that diabetes influences human weight. Thus, thiazolidinediones, being the main drug for diabetes treatment, lowered glucose and insulin level that led to insulin sensitivity. But, this was one of the main reasons for weight gaining (Banerjee and Lazar 219). Thus, it may be concluded that treating diabetes may cause obesity.

The increased insulin resistance leads to inability of the organism to the function properly. Thus, the glucose level increases, and it is impossible to cope with the problem until insulin resistance is not decreased. Some scientists proved that insulin resistance and diabetes are caused by diet-induced obesity. It was proven that “mice on a high-fat diet exhibited a strong positive correlation between body weight and blood glucose” (Banerjee, et al 1195).

Answering the question how resistin desensitizes insulin receptors and to what effect, the main idea of the insulin resistance and the necessity to decrease it should be considered. Insulin resistance, as it has already been mentioned, is an inability of target tissues to perceive insulin in a proper way. This cause glucose increase which leads to diabetes problems. Resistin occurs in adipose tissues and prevents glucose intolerance that, in its turn, decreases the level of insulin that makes the organism more sensitive to this hormone (Steppan and Lazar 19).

Many scientists and investigators in the sphere of diabetes noticed that resistin is the hormone which unites obesity and diabetes (Steppan et al. 307; Banerjee and Lazar 218; Banerjee et al. 1195). The endocrine role in those processes in huge as it supports glucose homeostasis maintaining (Banerjee et al. 1195). The levels of resistin which circulates may be decreased by means of drugs of thiazolidinedione class. At the same time, this level may be decreased with obesity. Insulin impact was better on mice which supported diet-induced obesity. Normal mice being treated with resistin experienced the glucose intolerance and reduction of insulin perception.

It was also proven that “Insulin-stimulated glucose uptake by adipocytes is enhanced by neutralization of resistin and is reduced by resistin treatment” (Steppan et al. 307) which shows link between obesity and diabetes. The problem of causality between obesity and diabetes is perfectly seen ion the paradox which involves resistin, adipose tissues, obesity and thiazolidinediones which has been considered above (Banerjee and Lazar 218).

Conclusion: Research Exploring Resistin Function in Mice and Humans

In the light of the problem, the research has been conducted which explored resistin function in mice and humans. McTernan et al. conducted a research of resistin function and tried to relate the results of the research in the relation to mice to those explored in humans (6098). The authors state that being quite sure in the influence of resistin on mice, the effect on humans remain rather controversial in the question of its influence on human weight. The results about the level of this hormone in human adipose tissues are rather conflicting, while the experiments on mice show the resistin is concentrated in adipose tissues.

The research was conducted in vitro with the purpose to show the concentration of resistin in diabetic issues, to define the insulin and rosiglitazone effect on resistin level and to “examine the functional effects of recombinant human resistin on glucose and lipid metabolism in vitro” (McTernan 6099). It is impossible to overestimate the role of this research as if it is possible to regulate the glucose level by means of resistin (thiazolidinediones is not really appropriate as it functions in a proper way but still people gain weight), the problem of diabetes treatment could have been solved. The regulation of the level of resistin in human adipose tissues may help increase the insulin sensitivity. Still, to be sure in the positive effect of all the issues mentioned above, much research should be conducted in the sphere to eliminate any unexpected consequences which may occur due to the environment and other factors.


Banerjee, Ronadip R, and Mitchell A Lazar. “Resistin: molecular history and prognosis.” Journal of Molecular Medicine 81.4 (2003): 218-226. Print.

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Hartman, Helen B., et al. “Mechanisms Regulating Adipocyte Expression of Resistin.” The Journal of Biological Chemistry 277.22 (2002): 19754-19761. Print.

Li, Fang-Ping. “Effects of resistin expression on glucose metabolism and hepatic insulin resistance.” Endocrine 35.2 (2009): 243-251. Print.

Liu, You, et al. “Effects of over-expressing resistin on glucose and lipid metabolism in mice.” Journal of Zhejiang University Science B 9.1 (2008): 44-50. Print.

Luo, Zhaofan. “Resistin induces insulin resistance by both AMPK-dependent and AMPK-independent mechanisms in HepG2 cells.” Endocrine 36.1 (2009): 60-69. Print.

McTernan, Philip G., et al. “Resistin and Type 2 Diabetes: Regulation of Resistin Expression by Insulin and Rosiglitazone and the Effects of Recombinant Resistin on Lipid and Glucose Metabolism in Human Differentiated Adipocytes.” The Journal of Clinical Endocrinolonogy Metabolism 88.12 (2003): 6098-6106. Print.

Pravenec, Michael, et al. “Transgenic And Recombinant Resistin Impair Skeletal Muscle Glucose Metabolism In The Spontaneously Hypertensive Rat.” The Journal of Biological Chemistry 278.46 (2003): 45209-45215. Print.

Steppan, Claire M. and Mitchell A. Lazar. “Resistin and obesity-associated insulin resistance.” TRENDS in Endocrinology & Metabolism 13.1 (2002): 18-23. Print.

Steppan, Claire M., et al. “The hormone resistin links obesity to diabetes.” Nature 409.6818 (2001): 307-312. Print.

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NursingBird. "Resistin and Its Potential Effects on Insulin Resistance." January 6, 2023.