Improvement of Systemic Adipokines and Adipokine Hepatic Gene Expression After Laparoscopic Sleeve Gastrectomy

Abstract

Introduction and Aim:

Obesity is characterized by low-grade inflammation, which is depicted by an increase of proinflammatory cytokines and a decrease of anti-inflammatory cytokines. This study was designed to assess the changes of systemic adipokines and adipokines hepatic gene expression after laparoscopic sleeve gastrectomy (LSG).

Patients and Methods:

The current prospective work included 81 obese cases for whom LSG was done. Paired liver biopsies, weight changes, biomarkers for glucose homeostasis, and hepatic enzymes in addition to serum and hepatic mRNA gene expression of adipocytokines (adiponectin, leptin, resistin, and pre-B cell enhancing factor [PBEF]/Nampt/visfatin) were assayed at baseline and at 18 months after LSG.

Results:

At the end of follow-up period, the results showed that LSG significantly improved markers of glucose homeostasis, hepatic enzymes, in addition to both serum and hepatic expression levels of different adipokines. Moreover, our analysis showed a direct positive correlation between initial body mass index (BMI) and serum leptin, as well as a negative correlation between BMI and serum adiponectin values.

Conclusion:

Weight loss-induced LSG is parallelized with substantial amendments of insulin resistance in addition to changes of the serum and hepatic gene expression of adipokines toward antidiabetic and anti-inflammatory profile.

Introduction

Obesity is an increasing public health disease that is notably linked to the most common etiologies of death—cardiovascular disease and malignancy.¹

The incidence of obesity is rising rapidly. It is believed that about one-third of the world's people are now either overweight or obese.² In addition, this epidemic is largely linked to insulin resistance, abnormal lipid profile, and type 2 diabetes mellitus (T2DM).³

Obesity results in a state of low-grade chronic inflammation. This state is characterized by an increase of proinflammatory cytokines such as leptin and resistin while at the same time decrease of anti-inflammatory cytokines such as adiponectin.⁴

Adiponectin is a well-established adipokine that plays its role through the peripheral metabolic organs (liver and muscle). Serum concentrations of adiponectin diminish with increasing fat mass. The synthesis of this adipocytokine is thought to be a hallmark of healthy adipocyte function because dysregulation of this adipokine is highly linked to metabolic disorders of obesity and T2DM.⁵

Leptin is another adipokine that increases with adipose tissue expansion.⁶ It enhances energy expenditure and reduces hepatic gluconeogenesis and insulin resistance.⁷ Hyperleptinemia in fatty cases does not decrease food intake or guard against the occurrence of adiposity.⁸

Resistin is a cysteine-rich adipokine induced during adipogenesis. Resistin is suggested as a link between adiposity and T2DM as it can affect different stages in the insulin-signaling pathway, resulting in insulin resistance.⁹ Previous study demonstrated that adipose tissue from obese diabetic patients exhibited raised values of resistin mRNA expression.¹⁰ Besides, researches showed elevated serum resistin values in obese cases in comparison with lean cases.¹¹

Pre-B cell colony enhancing factor (PBEF)/NAMPT/visfatin is a relatively new adipokine. Its biological roles are primarily proinflammatory as it enhances a lot of proinflammatory adipocytokines. Subjects with nonalcoholic fatty liver disease (NAFLD) have raised serum levels of PBEF/Nampt/visfatin. Significant weight reduction may result in a decline in serum concentrations and decreased hepatic gene expression.¹²

Bariatric operations are believed to be one of the most efficient strategies for the management of obesity. Recent researches have added to our comprehension about the mechanisms by which bariatric surgery affects adipocytokines, metabolism, and energy homeostasis.¹³

Laparoscopic sleeve gastrectomy (LSG) is nowadays the most commonly performed bariatric surgery in many parts of the world. The metabolic effects of LSG on different adipocytokines has yet to be accurately defined.¹⁴

This study was designed to characterize the changes of systemic adipokines and adipokines hepatic gene expression after LSG in a cohort of patients.

Patients and Methods

Patient selection

The current prospective study included obese cases for whom LSG was done. We adopted the STrengthening the Reporting of OBservational studies in Epidemiology (STROBE) instructions during the implementation of this study.

The local institutional review board approved the protocol of the study before starting. Included patients gave written informed consent at all appropriate stages of the study (before LSG, for research inclusion, for intraoperative wedge liver biopsies, and ultrasound-assisted true-cut liver biopsies at 18 months after surgery).

Criteria for inclusion into the study included those all set cases with body mass index (BMI) >40 or >35 kg/m² with other associated diseases such as T2DM or elevated blood pressure, patients encouraged for treatment and follow-up, those who failed to attain proper weight after adoption of nonsurgical strategies, ages between 18 and 60 years, and at last those cases with no endocrine causes for adiposity.

Confirmation of diabetes was done using the criteria of American Diabetes Association criteria (glycated hemoglobin [HbA1C] >6.5% or fasting blood sugar >126 mg/dL or 2-h plasma glucose >200 mg/dL during an oral glucose tolerance test).¹⁵

Criteria for exclusion included patients who are not fit for anesthesia, previous bariatric operation, gestation, or lactation at the screening. Besides, cases with secondary causes of liver disorders such as viral, alcohol, autoimmune, or drug induced were excluded from the study.

Preoperative evaluation

Initial assessment comprised the detailed history and clinical assessment, including height, weight, BMI, and amount of weight loss (in kg) that could be achieved by LSG.

Baseline investigations included alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), alkaline phosphatase, and markers for glucose homeostasis. Subjects were decided for LSG after multispecialty group assessment, including surgeons, bariatric specialists, psychiatrists, and dietitians.

Liver biopsy

Cases involved in this study underwent liver biopsies (wedge biopsy at the baseline during LSG and ultrasound-assisted true-cut biopsy at 18 months postoperative). Biopsies were settled in 10% neutral buffered formalin then put in paraffin blocks. Five-micrometer-thick slices were snipped and stained with hematoxylin and eosin.

Laboratory analysis

Venous blood samples were obtained after 8 h of fasting, and serum was collected by centrifugation at 1200 relative centrifugal force for 0.25 hour at 4°C and kept at −80°C. Serum samples were also collected at 18 months after LSG.

Serum insulin and serum adiponectin were assessed employing a radioimmunoassay technique (insulin-Phadeseph Insulin RIA; Pharmacia and Upjohn Diagnostics AB, Uppsala, Sweden and adiponectin; Linco Research, St. Charles, MO). Serum leptin was measured employing a human leptin enzyme-linked immunosorbent assay (ELISA) from R&D Systems (Minneapolis, MN). Serum PBEF/Nampt/visfatin levels were measured in duplicates employing a human “visfatin” (C-terminal) enzyme immunoassay (Phoenix Pharmaceuticals, Belmont, CA). Resistin was assessed with an ELISA from BioVendor (Modrice, Czech Republic). Other biochemical laboratories were performed using automated analyzers. Insulin resistance was calculated by the homeostasis model assessment index as follows: HOMA IR = fasting insulin (mU/L) × plasma glucose (mmol/L)/22.5.¹⁶

RNA extraction and quantitative real-time polymerase chain reaction

A modified acid guanidinium–phenol–chloroform method (Trizol reagent, Invitrogen, Paisley, Scotland, UK) was employed to extract total RNA from snap-frozen liver biopsies. Total RNA was quantitated photometrically, and random hexamers (Roche, Basel, Switzerland) and Moloney murine leukemia virus (M-MLV) reverse transcriptase (Invitrogen, Paisley, Scotland, UK) were employed to reverse transcribe 1 μg of total RNA based on the manufacturer's instructions. Twenty-five microliter quantitative PCRs were performed employing qPCR or mesa green master mixes (Eurogentec, Seraign, Belgium) in 45 cycles of 95°C for 30 s and 60°C for 1 min on an Mx3000 quantitative PCR system (Stratagene, Amsterdam, The Netherlands). Primer Express software (Perkin-Elmer Applied Biosystems, Warrington, UK) was employed to design oligonucleotide primers and TaqMan probes. For endogenous controls, predesigned TaqMan control reagents (Applied Biosciences, Foster City, CA) were employed to define mRNA expression of glyceraldehyde-3-phosphate dehydrogenase. Primers included are given in Table 1.

Table 1.

Primer List

Target	Sequence 5′–3′
Adiponectin (Acrp30)
Forward	AGA TGG CAC CCC TGG TGA G
Reverse	GGG TAC TCC GGT TTC ACC G
Probe	AAA GGA GAT CCA GGT CTT ATT GGT CCT AAG GGA
Leptin
Forward	CAT TTC ACA CAC GCA GTC AGT CT
Reverse	CAG TGT CTG GTC CAT CTT GGA TAA
Resistin
Forward	ATC AAT GAG AGG ATC CAG GAG G
Reverse	TCC AGG CCA ATG CTG CTT A
Probe	GCC CGG CTC CCT AAT ATT TAG GGC A
PBEF/Nampt/visfatin
Forward	GGT CTG GAA TAC AAG TTA CAT GAT TTT G
Reverse	TTG AAG TTA ACC AAG TGA GCA GAT G
Probe	TCT CTT CCC AAG AGA CTG CTG GCA TAG G

PBEF, pre-B cell enhancing factor.

Statistical analysis

Statistical Package for Social Sciences (SPSS, version 23) was employed for Statistical analysis. Kolmogorov–Smirnov and Shapiro–Wilk tests of normality were employed to define the suitable analytic test. Descriptive statistics (means and standard deviations, median and interquartile range, or frequency and percentages) were calculated for the collected variables. Differences between the baseline and follow-up data were tested by paired Student's t-test or Wilcoxon rank test as appropriate. Correlation coefficients were calculated using Spearman's method. A p-value <0.05 was considered statistically significant.

Results

At the start of the study, the work comprised 152 cases for whom serum and hepatic mRNA gene expression levels of adipocytokines were assayed. Seventy-one cases did not undergo the follow-up serum and/or hepatic mRNA gene expression of adipocytokines after 1.5 years, and so, at last, the study included 81 cases. Of these studied cases, 54% were males. The mean age of the studied cases was 43.25 ± 6.38 years, whereas the mean BMI was 43.99 ± 4.24 kg/m².

Patients' demographics are demonstrated in Table 2.

Table 2.

Clinical and Biological Characteristics at Baseline and After 18 Months Postsurgery

	Before weight loss (n = 81)	After 18 months postsurgery (n = 81)	p
Mean BMI (SD)	43.99 (4.24)	34.16 (2.65)	<0.001^**
Mean weight (SD)	122.95 (13.92)	95.42 (9.39)	<0.001^**
Mean height (SD)	167.11 (6.42)
ALT (U/L)	38 (11)	25 (9)	<0.001^**
AST (U/L)	32 (7)	23 (7)	<0.001^**
GGT (U/L)	39 (11.5)	28 (8)	<0.001^**
ALP, mean (SD)	62.40 (7.34)	61.52 (6.98)	<0.001^**
Glucose (mg/mL)	109 (23.50)	100 (21.50)	<0.001^**
HbA1C, mean (SD)	6.32 (0.84)	5.61 (0.56)	<0.001^**
Insulin (mU/L)	21 (3)	12 (2)	<0.001^**
HOMA index	5.7 (1.30)	2.90 (0.70)	<0.001^**

p value <0.001 highly significant.

Values are given as median (interquartile range). Wilcoxon signed rank test or paired Student's t-test was used to determine differences between pre- and postsurgery. Demographic variables are expressed as mean (SD).

ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; GGT, gamma glutamyl transferase; HbA1C, glycated hemoglobin; HOMA, homeostatic model assessment; SD, standard deviation.

This study showed a statistically highly significant decrease in weight from 122.95 ± 13.92 kg at baseline to 95.42 ± 9.39 kg at the end of the follow-up period (p < 0.001). Similarly, there was a statistically highly significant decrease in BMI from 43.99 ± 4.24 kg/m² to 34.16 ± 2.65 kg/m² (p < 0.001).

At baseline, T2DM was diagnosed in 13 cases, whereas after completion of the follow-up period, the number decreased to 8 cases, with no new encountered cases. In addition, this study showed a statistically highly significant decrease of fasting glucose (p < 0.001), HbA1C (p < 0.001), insulin levels (p < 0.001), and HOMA index (p < 0.001) (Table 2).

Regarding hepatic enzymes, this study demonstrated a statistically highly significant decrease of ALT (p < 0.001), AST (p < 0.001), and GGT (p < 0.001) at the end of the follow-up period (Table 2).

Adipokines

Adiponectin before and after surgery

LSG-induced weight loss was associated with statistically highly significant elevations in serum adiponectin values. The values increased from 7.45 ± 0.44 μg/mL preoperatively to 8.53 ± 0.59 μg/mL at 18 months after surgery (p < 0.001). Besides, there were statistically highly significant elevations of hepatic adiponectin mRNA gene expression from 0.43 ± 0.32 at the baseline to 0.95 ± 0.54 at 18 months post-LSG (p < 0.001).

Leptin before and after surgery

Our analysis showed statistically highly significant reductions of serum leptin levels from 27.96 ± 0.75 ng/mL at base line to 14.39 ± 1.14 ng/mL at 18 months postoperative (p < 0.001), whereas the values of hepatic leptin mRNA expression were comparable between pre- and postoperation (7.38 ± 0.90 vs. 7.44 ± 0.87, p = 0.36).

Resistin before and after surgery

This study demonstrated a statistically highly significant decrease of serum resistin levels from 4.25 ± 0.14 μg/mL at the baseline to 3.39 ± 0.19 μg/mL at 18 months post-LSG (p < 0.001). Also, our study showed a highly statistically significant decline in hepatic resistin mRNA expression at 18 months post-LSG (16.23 ± 0.31 vs. 9.26 ± 1.71, p < 0.001).

PBEF/Nampt/visfatin before and after surgery

This study revealed statistically highly significant decline in serum PBEF/Nampt/visfatin at 18 months post-LSG (12.13 ± 0.99 vs. 6.38 ± 0.83, p < 0.001). Similarly, a notable decrease was observed in hepatic PBEF/Nampt/visfatin mRNA expression at 18 months postsurgery (12.13 ± 0.99 vs. 6.38 ± 0.83, p < 0.001).

Correlations

We found that initial BMI positively correlated with serum leptin (r = 0.79, p < 0.001). Whereas BMI negatively correlated with serum adiponectin (r = −0.74, p < 0.001). However, there were no significant correlations between BMI and hepatic leptin mRNA expression (r = 0.16, p = 0.16), hepatic adiponectin mRNA expression (r = −0.03, p = 0.77), serum resistin (r = 0.15, p = 0.17), hepatic resistin mRNA expression (r = 0.01, p = 0.93), serum PBEF/Nampt/visfatin (r = 0.01, p = 0.90), and hepatic PBEF/Nampt/visfatin mRNA expression (r = −0.03, p = 0.81).

Insulin levels negatively correlated with initial serum adiponectin levels (r = −0.22, p = 0.046) and positively correlated with initial hepatic resistin gene expression (r = 0.24, p = 0.03). No significant correlations were found between glucose, insulin, and HOMA indices with baseline serum resistin and PBEF/Nampt/visfatin.

Table 3 gives predictive value of adipokines at baseline on weight loss and BMI at 18 months after surgery. Table 4 gives correlations between circulating adipokine levels and their respective hepatic expression.

Table 3.

Predictive Value of Adipokines at Baseline on Weight Loss at 18 Months After Surgery

	Amount of weight loss (kg)
Adiponectin serum level change
Correlation coefficient	0.036
p	0.748
n	81
Hepatic adiponectin mRNA expression change
Correlation coefficient	0.042
p	0.711
n	81
Leptin serum level change
Correlation coefficient	0.480
p	<0.001^**
n	81
Hepatic leptin mRNA expression change
Correlation coefficient	−0.158
p	0.160
n	81
Resistin serum level change
Correlation coefficient	−0.198
p	0.077
n	81
Hepatic resistin mRNA expression change
Correlation coefficient	0.168
p	0.135
n	81
PBEF/Nampt/visfatin serum level change
Correlation coefficient	−0.447
p	<0.001^**
n	81
Hepatic PBEF/Nampt/visfatin mRNA expression change
Correlation coefficient	−0.083
p	0.459
n	81

p value <0.001 highly significant.

Table 4.

Correlations Between Circulating Adipokine Levels and Their Respective Hepatic Expression

	Initial adiponectin serum levels (μg/mL)	Adiponectin serum levels after 18 months (μg/mL)	Serum leptin levels (ng/mL)	Serum leptin levels after 18 months (μg/mL)	Initial serum resistin levels (μg/mL)	Resistin serum levels after 18 months (μg/mL)	Initial serum PBEF/Nampt/visfatin (pg/mL)	Serum PBEF/Nampt/visfatin after 18 months (pg/mL)
Initial hepatic adiponectin mRNA expression
Correlation coefficient	0.014	−0.048	0.032	0.034	−0.040	−0.160	0.104	0.171
p	0.902	0.670	0.775	0.762	0.724	0.154	0.355	0.127
N	81	81	81	81	81	81	81	81
Hepatic adiponectin mRNA expression after 18 months
Correlation coefficient	0.097	0.100	−0.061	−0.064	−0.046	−0.126	0.290	0.329
p	0.391	0.374	0.587	0.570	0.686	0.262	0.009^*	0.003^*
N	81	81	81	81	81	81	81	81
Initial hepatic leptin mRNA expression
Correlation coefficient	−0.226	−0.144	0.137	0.120	−0.020	0.028	−0.233	−0.352
p	0.043^*	0.198	0.224	0.287	0.863	0.802	0.036^*	0.001^**
N	81	81	81	81	81	81	81	81
Hepatic leptin mRNA expression after 18 months
Correlation coefficient	−0.176	−0.065	0.084	0.122	−0.015	0.074	−0.094	−0.162
p	0.115	0.562	0.457	0.278	0.896	0.512	0.402	0.148
N	81	81	81	81	81	81	81	81
Initial hepatic resistin mRNA expression
Correlation coefficient	0.222	0.198	−0.174	−0.217	−0.067	−0.012	−0.116	−0.059
p	0.046^*	0.076	0.121	0.052	0.555	0.915	0.304	0.600
N	81	81	81	81	81	81	81	81
Hepatic resistin mRNA expression after 18 months
Correlation coefficient	−0.033	0.019	0.077	−0.002	0.028	0.096	−0.063	0.008
p	0.772	0.867	0.493	0.986	0.805	0.393	0.578	0.942
N	81	81	81	81	81	81	81	81
Initial hepatic PBEF/Nampt/visfatin mRNA expression
Correlation coefficient	−0.108	−0.024	0.141	0.131	−0.073	0.043	−0.048	−0.001
p	0.339	0.828	0.208	0.242	0.519	0.706	0.672	0.993
N	81	81	81	81	81	81	81	81
Hepatic PBEF/Nampt/visfatin mRNA expression after 18 months
Correlation coefficient	0.034	0.119	0.002	0.029	−0.082	0.014	−0.015	0.006
p	0.763	0.289	0.984	0.797	0.465	0.902	0.893	0.958
N	81	81	81	81	81	81	81	81

p value <0.05 significant, ^**p value <0.001 highly significant.

Discussion

In obese subjects, the excess number of adipocytes synthesizes and secretes several inflammatory mediators. These mediators lead to a proinflammatory condition in addition to increased oxidative stress. This proinflammatory status is thought to be the primary mechanism for the pathogenesis of cardiovascular diseases, atherosclerosis, insulin resistance, and metabolic syndrome.¹⁷

In this study, we evaluated the hypothesis that alterations in serum and hepatic mRNA gene expression of different adipokines after LSG-induced weight loss are associated with the improvement of metabolic profile.

This study revealed that weight loss-induced LSG was associated with significant resolution in insulin resistance, plasma glucose, and liver functions in addition to serum and hepatic expression of the studied adipokines. Besides, our study revealed a positive relationship between initial BMI and serum leptin and a negative correlation between initial BMI and serum adiponectin values. The results of this study may enrich the published literature on the positive impact of weight loss-induced LSG on adipocytokines profile in obese cases.

To comprehend the impact of these results, they should be explained within the pathophysiological roles of these adipokines.

Adiponectin is a hormone synthesized and secreted by adipocytes. This adipokine has gained attention as it has beneficial effects on inflammatory status,¹⁸ T2DM, and insulin resistance.¹⁹ Adiponectin is believed to possess an intimate relation with multiple aspects of the metabolic syndrome.²⁰

This study revealed that both serum and hepatic expression levels of adiponectin increased after LSG. These changes may interpret the simultaneous improvement of blood glucose and insulin resistance in the studied subjects.

These results agree with those obtained by Hosseinzadeh-Attar et al., who showed a significant increase in adiponectin levels after metabolic surgery.²¹ Yet, it should be observed that they studied adiponectin changes after 6 weeks only, in our study, we showed more long-term maintained effects of the surgery after 18 months.

Leptin is another adipokine that is synthesized and secreted by adipocytes. It is well known that values of serum leptin are correlated with the degree of obesity, yet it should be noted that the body fat mass is not the only regulator of serum levels. Regulation of leptin is also affected by dietary lifestyle and recent weight gain.²²

Leptin has a vital role in energy homeostasis and food intake regulation.²³ High leptin levels, as evidenced by previous study, may increase the risk of elevated blood pressure, ischemic heart disease, and thromboembolic manifestations.^24–26 Leptin levels tend to decrease after weight loss-induced bariatric surgery.²²

In addition, previous study revealed that adiponectin/leptin ratio might be an indicator of early atherosclerosis as it was intimately related to intima-media thickness of the common carotid artery.²⁷

In this study, it was found that decreased leptin serum values were parallelized with LSG-induced weight loss. In addition, our study showed a positive relationship between BMI and values of serum leptin. The results were reproduced by previous studies.^23,28 Not far from this, Kelly et al. showed that the risk of T2DM could be decreased by weight loss-induced metabolic surgery, and this may occur through the improvement of inflammatory status and adipocytokine profile (particularly reduced values of serum leptin).²⁹

Leptin can be expressed in triggered hepatic stellate cells, which may, therefore, be a source of leptin tissue and serum levels, giving a share in the pathophysiological mechanisms of chronic liver disease.³⁰ Our analysis showed that values of hepatic leptin mRNA expression were comparable before and after surgery, and these results agree with Moschen et al. who found that leptin hepatic mRNA expression did not change after weight loss-induced bariatric surgery.²³

These results may suggest that, although leptin may be expressed by the liver, it is mainly expressed and predominantly secreted by mature white adipocytes. Therefore, contribution of potential serum levels from the liver may be limited.

Resistin is an adipocytokine that is secreted by adipose tissue. It enhances hepatic gluconeogenesis and insulin resistance.^31,32 Previous report suggested that it has a role in the inflammatory status related to obesity through stimulation of the NF-κB pathway and synthesis and secretion of interleukin-6 and tumor necrosis factor-α.³³ In addition, it can stimulate the SOC-3 enzyme, a regulator of cytokine signaling, leading to insulin resistance.^31,32 In this study, we showed a positive correlation between hepatic resistin mRNA expression and insulin levels. In addition, it was revealed that significant weight loss after LSG was parallelized by a decrease in serum resistin values.

In review of the literature, we will find contradictory results regarding the impact of metabolic surgery on serum resistin levels. Some researchers showed a notable decrease in values of serum resistin postmetabolic surgery^34–36; in contrast, other researchers did not reach the same results.^37–39 Adding to this dilemma, this study did not show a notable correlation between BMI and values of serum resistin. More extensive study is warranted to confirm the impact of metabolic surgery on values of serum resistin.

Resistin hepatic gene expression is thought to be low in sound human liver, yet raised in cases of inflammatory changes and hepatic fibrosis. The upregulation of resistin during chronic liver disease was assured by immunohistochemistry.⁴⁰ Our analysis showed that reduced weight after bariatric surgery was associated with significant reductions in resistin hepatic mRNA expression, and these results agree with a recent study that demonstrated a substantial decline in hepatic mRNA expression of resistin after considerable weight loss in severely obese subjects.⁴¹

PBEF/Nampt/visfatin is one of the recently discovered adipokines. It was first described in 2005.⁴² Adipose tissue, immunocytes, and hepatocytes are the major sources of this adipokine.⁴³ It was thought that PBEF/Nampt/visfatin has a role in enhancing the proinflammatory status as its levels are raised in different inflammatory conditions as acute lung injury,⁴⁴ psoriasis,⁴⁵ and septicemia.⁴⁶ Obese cases with NAFLD have notably higher levels of serum and hepatic gene expression of visfatin than cases with healthy livers.⁴⁷

This study revealed substantial decreases in PBFE/Nampt/visfatin serum levels and hepatic mRNA expression post-LSG. These results agree with previous research, which demonstrated decreased values of PBFE/Nampt/visfatin after metabolic surgery in overweight patients⁴⁸ and postlaparoscopic adjustable gastric banding.³³ Another study found that weight loss was associated by a decline in visfatin serum and hepatic gene expression levels.²³

It deserves to note that this study has some limitations. Diverse nutritional and physical lifestyles could be a confounding factor in this study. In addition, this study had no control group because of ethical causes. It is also worth to mention that most of the adipokines assessed in this study have their primary expression in the adipose tissue rather than in the liver.

In conclusion, weight loss-induced LSG is parallelized with substantial amendments of insulin resistance in addition to changes of the serum and hepatic gene expression of adipokines toward antidiabetic and anti-inflammatory profile.

Novelty of the study

To the best of our information, the scientific research on this topic (serum and hepatic expression of adipokines post-LSG) is scarce in the literature. Besides, this study is characterized by a quite long period of follow-up, the point that may make our work fairly unique, as most previous studies did not adopt such long periods of follow-up.

Furthermore, study of changes of these adipocytokines may provide new horizons that shall help to explore new therapeutic modalities in chronic inflammatory conditions related to obesity and other aspects of the metabolic syndrome.

Footnotes

Author Disclosure Statement

No competing financial interests exist.

Funding Information

No funding was received.

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