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Year : 2022  |  Volume : 8  |  Issue : 2  |  Page : 95-98

Serum leptin and adiponectin in metabolic syndrome: A brief review

Department of Biochemistry, Santosh Medical College and Hospital, Santosh Deemed to be University, Ghaziabad, Uttar Pradesh, India

Date of Submission22-Nov-2022
Date of Acceptance24-Nov-2022
Date of Web Publication11-Jan-2023

Correspondence Address:
Juhi Aggarwal
Department of Biochemistry, Santosh Medical College and Hospital, Santosh Deemed to be University, Ghaziabad - 201 009, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/sujhs.sujhs_36_22

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Metabolic syndrome in modern times is a global health issue in the world including India. Its prevalence in the population is following a crescendo pattern. By knowing metabolic syndrome not only we are able to diagnose it in an early and proper manner but can also promote the prevention program. Leptin is a hormone which is mainly synthesized in the white adipose tissue. Leptin level in blood is directly proportional to total adipose tissue mass. In the present study, the association of serum leptin and adiponectin with the components of metabolic syndrome was evaluated. Patients with metabolic syndrome had higher levels of leptin and low levels of adiponectin than Non-Metabolic syndrome (MS) Subjects. We have also found that as compared to the females, the male had a higher possibility of metabolic syndrome.

Keywords: Adiponectin, diabetes mellitus, leptin, metabolic syndrome, obesity

How to cite this article:
Aggarwal J, Midha U, Batra J. Serum leptin and adiponectin in metabolic syndrome: A brief review. Santosh Univ J Health Sci 2022;8:95-8

How to cite this URL:
Aggarwal J, Midha U, Batra J. Serum leptin and adiponectin in metabolic syndrome: A brief review. Santosh Univ J Health Sci [serial online] 2022 [cited 2023 May 30];8:95-8. Available from: http://www.sujhs.org/text.asp?2022/8/2/95/367571

  Introduction Top

Metabolic syndrome is a cluster of various metabolic abnormalities and physical conditions which may multiply a person's risk for heart disease, diabetes, and stroke. By knowing metabolic syndrome not only we are able to diagnose it in an early and proper manner but can also promote the prevention program. In modern times, metabolic syndrome is a major public health issue and may be an important reason behind the global epidemics of cardiovascular disease (CVD) and type 2 diabetes. It has been observed that metabolic syndrome patients are having a higher risk of myocardial infarction and stroke. The risk of death from such events in metabolic syndrome patients is two times high as compared to those without metabolic syndrome.[1] Furthermore, premature deaths and disabilities resulting from metabolic syndrome have increased the burden on health budgets in both developed and developing nations.

Hanefield and Leonhardt, in 1981, were the first to use the term metabolic syndrome and described it as a combination of diabetes mellitus, obesity, gout, hypertension, hyperlipoproteinemia, fatty liver, and cholelithiasis in addition to increased incidence of heart disease in 1985.[2] Modan et al. demonstrated insulin resistance syndrome as a common pathophysiological association for hypertension, obesity, and glucose intolerance.[3]

In the modern era, there is a trend for chronic diseases such as diabetes and CVD and decreasing impact of acute infectious disease.[4] The World Health Organization and epidemiologists in India have been sounding an alarm on the rapidly rising burden of CVD in past few years. By 2020, it is assumed that CVD will be the most common cause of disability and with 2.6 million deaths in India.[5]

CVD and diabetes are preceded by a constellation of risk factors which are also the components of MS. The CVD and diabetes complications may also lead to renal failure, amputation, and blindness which increases the social and financial burden of disease.[6] By 2025, it is estimated that the incidence of diabetes will be twice and there will be an increase in CVD-related morbidity and mortality. It will further enhance the burden on health care. In 2003, approximately 7.2% of total health expenditure was due to diabetes in the age group of 20–79 years in 25 European countries (≈70 billion international dollars).[7]

In addition, a long-term complication associated with metabolic syndrome can be identified at an early stage, and through lifestyle modification, we can delay or even prevent the development of serious health problems.

Leptin is a 16-kDa adipocyte-derived hormone that circulates in the serum in the free and bound form. Positional cloning of ob/ob mouse model of obesity, which is deficient in leptin, led to the discovery of the leptin gene (ob gene).[8]

It acts on receptors in the lateral hypothalamus to inhibit hunger. Leptin is opposed by the actions of the hormone ghrelin (the hunger hormone). Thus, it plays an important role in the regulation of the storage of fat in the body. Leptin level in blood is directly proportional to total adipose tissue mass. Therefore, in obesity increase in adipose tissue mass increases the serum leptin level. In obesity, a decreased sensitivity to leptin occurs, resulting in an inability to detect satiety despite high energy stores. Leptin receptors are expressed in the hypothalamus and hippocampus.

Another adipokine that is synthesized by both brown and white adipose tissue is adiponectin. It plays an important role in the regulation of insulin sensitivity and tissue inflammation and circulates in a very high concentration in the blood with different molecular weight forms and is produced by multimerization. The high-molecular-weight complexes act mainly in the liver as per the data in the studies. Adiponectin is a protein hormone which is exclusively secreted in the adipose tissue, however, in pregnancy, the placenta is also producing it.

It plays a role in the regulation of glucose levels and fatty acid oxidation. It has antiatherosclerotic, antidiabetic, and anti-inflammatory properties, and therefore, it is a potential indicator of metabolic complications. A low level of serum adiponectin is associated with decreased insulin sensitivity, increased body mass index (BMI), increased inflammatory markers, and less favorable lipid profile. Hypoadiponectinemia is associated with an increased risk of CVD, diabetes, atherosclerosis, nonalcoholic fatty liver, obesity, and metabolic syndrome.

  Discussion Top

Metabolic syndrome is a major challenge in terms of public health. One of the problems is its association with heart disease and the risk of which may increase many folds. Now, in the modern era, it became a focus of attention. The important reason for an increased rate of metabolic syndrome in the population is lifestyle modification. Less physical activities, improper eating habits, and more stress have increased the trend of obesity in the community. Metabolic syndrome is characterized by a variety of features such as increased blood pressure, high cholesterol, triacylglycerol, insulin, and glucose in plasma. Other features are high intramuscular lipids, intramyocellular lipids, and increased risk of type 2 diabetes mellitus and cardiac disease. With time, it has been observed that the prevalence of obesity and metabolic syndrome has affected the younger population and it may be an epidemic in the future. Both metabolic syndrome and obesity are linked to visceral fats so detailed knowledge of their physiology and pathology can help us to understand the basic concepts and it may be useful in prevention and treatment also.

Preadipocytes are the precursor of lipid-assimilating adipocytes and information regarding them can be obtained by stromal vascular cell fraction. Heterogeneity in gender in terms of the prevalence of metabolic syndrome and it was found twice in males as compared to females in a study conducted by Sawant et al.[8] However, MS prevalence was 1.5–2 times higher in males than females in the other studies in India.[9]

The prevalence of MS in both males and females increases with age and the same finding in our study was found with a maximum of 31–40 years. Kelliny et al. had documented the same trend but maximum in the age group of 45–54 years.[10] The progressive increase in total adipocytes (usually denoted by BMI) is related to an increase in noncommunicable disease as found in population studies, however, finding of epidemiological studies has shown that there is a greater incidence and prevalence o of CVD, dyslipidemia, and type 2 diabetes as a function of increasing BMI. Individuals with the same BMI values may have remarkable heterogeneity.

A higher risk of type 2 diabetes and CVD has been found in individuals with equal obesity or overweight but with increased abdominal fat (determined by waist circumference). This finding is independent of the risk predicted by increased BMI. The computed tomography scan of visceral adiposity has clearly shown that individuals with excessive adipocytes have adverse alterations in metabolic risk profiles. Fasting hypertriglyceridemia in the presence of increased waist circumference is a useful marker of the possibility that increased girth is due to the deposition of visceral fat. Abdominal fat is made up of intra-abdominal and abdominal subcutaneous fat (Mårin et al.). Intra-abdominal fat, in turn, consists of visceral or intra-peritoneal (omental and mesenteric fat) and retroperitoneal fat delineation along the dorsal borderline of the intestine and the ventral surface of the kidney.[11]

Visceral fat is more resistant than subcutaneous fat to insulin. Therefore, insulin resistance may also increase with an increase in visceral fat. The latter response is also more to catecholamine, glucocorticoid, and lipolytic hormones. In response to the high level of insulin, visceral is unable to suppress the free fatty acid (FFA) levels through adipose tissue lipolysis.

FFA increases insulin resistance. Furthermore, continuous FFA entry to the liver may result in nonalcoholic fatty liver. There may be an increased risk of CVD, alteration in the levels of low-density lipoprotein cholesterol and high-density lipoprotein cholesterol (HDL-C), endothelial dysfunction, and vascular smooth muscle cell proliferation. High levels of FFA in nonadipose tissue may induce systemic inflammation and necrosis by producing structural abnormalities and damaging metabolites which in turn may increase the CVD risk.[12]

Among the parameters of IDF criteria, increased waist circumference is the most prevalent metabolic component in the Indian urban population. Low HDL-C and high triglyceride (TG) were the least prevalent components of metabolic syndrome in the same population. Almost the same finding, the increased waist circumference as most and elevated TG and least prevalent components were observed by Ogbera in the Nigerian population.[13]

Most of the patients with metabolic syndrome in our study had three components positive. The most common combination of components was increased waist circumference, elevated blood pressure, and high fasting plasma glucose levels. High TG levels and low HDL-C were the fourth most frequent component.

Adipose tissue is the site for the storage of most fats in the form of TG in the body and here the estrogens are synthesized from the androgens. It has been shown in research papers that these adipose tissues may also be the site of production of various types of adipocytokines such as leptin, adiponectin, adipsin, resistin, tumor necrosis factor-α, etc., which may be important for the balance of fat stores, homeostasis, and adaptation of the body to the different conditions (stress, infection, increase energy demanding situations, and starvation).[14]

There is more need to know about the mechanisms that are involved in the regulation and secretion of adiponectin and investigation has started already regarding this issue. Now, there is more focus on studies to know the effect of hormonal and environmental factors on the circulating levels of adiponectin in the whole body or its expression and secretion at the level of the cells. It has been seen in vivo that there is no active regulation on the secretion of adiponectin levels but the expression of it is relatively under acute regulation (4–6 hourly) through feeding or refeeding.[15]

In the adult, adiponectin circulating levels have an inverse correlation to adipose tissue mass.[16] Kistorp C et al.(2005) demonstrated that there is an inverse correlation between adiponectin levels and BMI.[20] Schober et al. in their study observed a negative correlation of adiponectin with waist circumference.[17] Wang et al. demonstrated a negative correlation of adiponectin levels with parameters of metabolic syndrome. These findings are in agreement with the present study also. A strong negative correlation was found in the current study between parameters of metabolic syndrome and adiponectin levels.[18]

From these findings, we can assume that leptin and adiponectin can be good diagnostic markers or possibly a predictor of metabolic syndrome. It has been seen in some recent studies that a stronger correlation between leptin: adiponectin (L:A) ratio or the inverse ratio (adiponectin: leptin) and metabolic syndrome on the one hand, than the association between leptin or adiponectin alone and MS on the other. In some other studies, however, the results are just the opposite. Mojiminiyi's and his coworker found adiponectin is a better marker of metabolic syndrome in diabetes than L:A ratio. Due to the above finding, the different criteria to define metabolic syndrome have been given with time. Gauthier et al.(2012) observed a positive correlation between L:A ratio of each criteria of metabolic syndrome.[19] Therefore, it can be said that metabolic syndrome is a condition which is associated with abnormal glucose and lipid profile, insulin resistance, hypertension, and android weight distribution. MS increases the risk of heart disease. In various populations, a link has been demonstrated between leptin, adiponectin, and metabolic syndrome in different studies.

  Conclusion Top

Higher adiponectin levels were associated with a lower risk of developing metabolic syndrome, whereas higher leptin levels and LA ratio were associated with an elevated metabolic syndrome incidence in both men and women. Continuous monitoring of adiponectin, leptin, and LA ratio could help detect high-risk individuals for metabolic syndrome. Furthermore, further investigation into patterns of serum adiponectin and leptin levels are associated with the risk of incident metabolic syndrome in a large population-based prospective study with a longer follow-up period.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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Modan M, Halkin H, Almog S, Lusky A, Eshkol A, Shefi M, et al. Hyperinsulinemia. A link between hypertension obesity and glucose intolerance. J Clin Invest 1985;75:809-17.  Back to cited text no. 3
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Sawant A, Mankeshwar R, Shah S, Raghavan R, Dhongde G, Raje H, et al. Prevalence of metabolic syndrome in urban India. Cholesterol 2011;2011:920983.  Back to cited text no. 8
Prabhakaran D, Chaturvedi V, Shah P, Manhapra A, Jeemon P, Shah B, et al. Differences in the prevalence of metabolic syndrome in urban and rural India: A problem of urbanization. Chronic Illn 2007;3:8-19.  Back to cited text no. 9
Kelliny C, William J, Riesen W, Paccaud F, Bovet P. Metabolic syndrome according to different definitions in a rapidly developing country of the African region. Cardiovasc Diabetol 2008;7:27.  Back to cited text no. 10
Mårin P, Andersson B, Ottosson M, Olbe L, Chowdhury B, Kvist H, et al. The morphology and metabolism of intraabdominal adipose tissue in men. Metabolism 1992;41:1242-8.  Back to cited text no. 11
Jensen MD. Role of body fat distribution and the metabolic complications of obesity. J Clin Endocrinol Metab 2008;93:S57-63.  Back to cited text no. 12
Ogbera AO. Prevalence and gender distribution of the metabolic syndrome. Diabetol Metab Syndr 2010;2:1.  Back to cited text no. 13
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Zhang Y, Matheny M, Zolotukhin S, Tumer N, Scarpace PJ. Regulation of adiponectin and leptin gene expression in white and brown adipose tissues: Influence of beta3-adrenergic agonists, retinoic acid, leptin and fasting. Biochim Biophys Acta 2002;1584:115-22.  Back to cited text no. 15
Hu E, Liang P, Spiegelman BM. AdipoQ is a novel adipose-specific gene dysregulated in obesity. J Biol Chem 1996;271:10697-703.  Back to cited text no. 16
Schober F, Neumeier M, Weigert J, Wurm S, Wanninger J, Schäffler A, et al. Low molecular weight adiponectin negatively correlates with the waist circumference and monocytic IL-6 release. Biochem Biophys Res Commun 2007;361:968-73.  Back to cited text no. 17
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Gauthier A, Dubois S, Bertrais S, Gallois Y, Aube C, F Gagnadoux, et al. The Leptin to Adiponectin Ratio is a Marker of the Number of Metabolic Syndrome Criteria in French Adults. J Metabol Syndro 1:101. doi:10.4172/jms.1000101.  Back to cited text no. 19
Kistorp C, Faber J, Galatius S, Gustafsson F, Frystyk J, Flyvbjerg A, et al. Plasma adiponectin, body mass index, and mortality in patients with chronic heart failure. Circulation. 2005;112:1756-62.  Back to cited text no. 20


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