Table of Contents    
Year : 2015  |  Volume : 6  |  Issue : 1  |  Page : 89-93  

Relationship between postprandial endotoxemia in nonobese postmenopausal women and diabetic nonobese postmenopausal women

1 Department of Clinical Biochemistry, Government College of Medicine, King Khalid University, Abha, Kingdom of Saudi Arabia
2 Head of Operations and Quality Manager Ekopath Metropolis, Guwahati, Assam, India

Date of Web Publication14-Jan-2015

Correspondence Address:
Dr. Gaffar Sarwar Zaman
Department of Clinical Biochemistry, Government College of Medicine, King Khalid University, Abha
Kingdom of Saudi Arabia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0976-9668.149098

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Background: We hypothesised that nonobese postmenopausal women (NoPoW) and diabetic NoPoW (DNoPoW) may be independently associated with postprandial endotoxemia. Materials and Methods: NoPoW and DNoPoW were evaluated for weight, eating habits, physical activity, body circumferences, fasting plasma glucose level, postprandial plasma glucose level, and insulin level. The lipopolysaccharide (LPS) levels and circulating LPS-binding protein (LBP) were determined in serum at fasting, 1 h, 2 h, 3 h, and 4 h after meal intake and their levels were co-related in 80 NoPoW and 80 DNoPoW. Results: Both DNoPoW group and NoPoW group showed a significant increase (P < 0.05) in LPS levels and circulating LBP in plasma after the meal intake, interestingly the increase was higher in the DNoPoW group. Conclusions: Elevated LPS and circulating LBP were associated significantly with DNoPoW group and NoPoW, especially after a meal intake. These findings suggested a role of LPS and LBP in postprandial systemic inflammation in DNoPoW group. Prospective studies are needed to confirm these results.

Keywords: Endotoxemia, lipopolysaccharide, lipopolysaccharide-binding protein, postmenopause

How to cite this article:
Zaman GS, Zaman F. Relationship between postprandial endotoxemia in nonobese postmenopausal women and diabetic nonobese postmenopausal women. J Nat Sc Biol Med 2015;6:89-93

How to cite this URL:
Zaman GS, Zaman F. Relationship between postprandial endotoxemia in nonobese postmenopausal women and diabetic nonobese postmenopausal women. J Nat Sc Biol Med [serial online] 2015 [cited 2021 Jan 19];6:89-93. Available from:

   Introduction Top

Lipopolysaccharide (LPS) is an endotoxin (molecular weight >100,000 Daltons) and is composed of two major parts, the hydrophobic lipid A portion and the hydrophilic polysaccharide portion (commonly called the "O" region). Circulating endotoxin may derive from bacteria or gut microflora causing either overt acute infections or common chronic inflammatory conditions or cardiometabolic abnormalities including obesity, insulin resistance, and diabetes. [1] Endotoxin circulates in the plasma of healthy human subjects at low concentrations (between 1 and 200 pg/Ml). [2],[3],[4],[5] However as the human gut is host to 100 trillion commensal organisms, which together contribute to an enteric reservoir of 1 g LPS, it is hypothesized that most of the circulating endotoxin may derive from the gut and that a small amount of commensally derived LPS may cotransit with dietary fat from the gut after a high-lipid meal, which thereby increases plasma endotoxin concentrations postprandially.

The increased cardiovascular disease (CVD) risk after menopause seems to be associated with the emergence of the features of metabolic syndrome. [6],[7] In fact, women with type 2 diabetes mellitus (T2DM), compared with age-matched nondiabetic women, exhibit several-fold higher rates of death-related to coronary artery disease, with event rates nearly identical to those observed in T2DM men. [8] Traditional cardiovascular risk factors cannot completely account for these sex differences in cardiovascular mortality. [9] Hence, more studies are needed to understand the precise influence of menopause in the risk for CVD, especially in diabetic patients, in order to achieve effective preventative and disease management strategies to reduce the CVD risk particularly in postmenopausal women. Estrogen exerts cardioprotective action by maintaining a high level of high-density lipoprotein cholesterol and lowering the low-density lipoprotein cholesterol and triglycerides. [10],[11],[12],[13] Loss of this protection after menopause may, therefore, be responsible for increased risk of developing CVD in postmenopausal women. [14],[15],[16],[17] Increases in body weight are associated with greater risks of type 2 diabetes, [18],[19],[20] and weight gain in postmenopausal women are of special concern. [21] Estrogen has remarkable effects on body fat distribution, and the decreased estrogen production after menopause is associated with increased total body fat, [22],[23] especially in the central/abdominal region. [24],[25]

   Materials and Methods Top

Patients inclusion and exclusion criteria

This study was conducted in accordance with the ethical rules of the Helsinki Declaration. The study was approved by the Ethics Committee of the hospital, and all women gave written informed consent. Prior to the study, participants were informed that their confidentiality would be maintained, and consent was obtained. Eighty nonobese postmenopausal women (NoPoW) and 80 diabetic NoPoW (DNoPoW) were selected for the study. For the 80 NoPoW patients were excluded if they had CVD, arthritis, acute inflammatory disease, infectious disease, renal disease, were receiving treatment for hyperlipidemia or diabetes or were taking medications that could influence gastric emptying or the absorption time. For the 80 DNoPoW, all the above criteria except diabetes cases were excluded.

Preparation of patients and sample collection

On the morning of the visit, blood pressure, weight, and height were measured, and compliance with dinner instructions was verified with a questionnaire. After that, each participant underwent a structured examination, which included an interview. Height, weight, waist circumference (WC) and hip measurements, a fasting venipuncture, and sequential determination of serum lipids were done. Height and weight were measured to the nearest 0.5 cm and 0.1 kg, respectively. Body mass index (BMI) was calculated as weight (kilogram) divided by height (in meter) squared. WC was determined to the nearest 0.1 cm using a measuring tape positioned at the midpoint between the lowest rib and the iliac crest and hips were measured at the largest gluteal circumference. These measurements were used to calculate the waist-to-hip ratio. Blood pressure was measured using a standard mercury sphygmomanometer. Blood samples were obtained from the antecubital vein and placed in vacutainer tubes. Postprandial blood samples were taken 1, 2, 3, and 4 h after the end of the study meal. Samples were centrifuged; serum was collected and stored at 20°C until analyzed. The diagnosis of DM was based on WHO criteria, [26] that is, a fasting plasma glucose level >7.0 mmol/L or >126 mg/dL, or a 2-h postprandial plasma glucose level >11.1 mmol/L or >200 mg/dL on more than one occasion, with symptoms of diabetes.

Serum LPS concentrations were measured by endotoxin assay, based on a Limulus amebocyte extract with a chromogenic Limulus amebocyte lysate (LAL) assay (QCL-1000, Lonza Group Ltd.). Samples were diluted in pyrogen-free water and heated at 70°C for 10 min to inactivate endotoxin-neutralizing agents that inhibit the activity of endotoxin in the LAL assay. Internal control of recovery calculation was included in the assessment. All samples were tested in duplicate. The endotoxin content was expressed as endotoxin units (EU)/mL. Exhaustive care was taken to avoid environmental endotoxin contamination and all material used for sample preparation, and the test was pyrogen-free. Plasma LPS-binding protein (LBP) levels were determined by a sandwich enzyme-linked immunosorbent assay Technology. Plasma samples were diluted at least 200 times and assayed according to the manufacturer's instructions. The assay has a sensitivity of 0.2 ng/ml. The intra-assay and inter assay coefficients of variation were <5 and <10%, respectively.

Statistical analysis

All data are presented as mean ± standard deviation and were analyzed using GraphPad prism version 5 (San Diego, California, USA). Differences between two groups were analyzed by Student's t-test, while multiple groups were compared using ANOVA, followed by Bonferroni's multiple comparison tests. P < 0.05 was considered as statistically significant.

   Results Top

The mean BMI values were 23.0 ± 1.4 kg/m 2 in NoPoW and 24.0 ± 2.1 kg/m 2 in DoPoW [Table 1]. The mean WCs were 74 ± 6.2 in DoPoW and 70.9 ± 7.1 in NoPoW. The mean systolic blood pressure (mmHg) was 115.6 ± 14.3 in DoPoW and 109.5 ± 16.4 in NoPoW, whereas the diastolic blood pressure (mmHg) was 78.9 ± 4.9 in DoPoW and 71.9 ± 11.8 NoPoW Compared with NoPoW, DoPoW were more likely to have higher values for WC, blood pressure, and glucose. Fasting plasma glucose and postprandial plasma glucose were in the range of 91 ± 11 and 132 ± 19 in NoPoW and 164 ± 17 and 258 ± 27 in DoPoW.
Table 1: Patient characteristics

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The mean plasma endotoxin (LPS) in NoPoW in EU/mL was 0.37, 0.44, 0.64, 0.59 and 0.57 at fasting, 1, 2, 3, and 4 h versus 0.39, 0.5, 0.72, 0.73 and 0.66 in the DoPoW during the same duration. The mean LBP μg/ml was 10.9, 14.6, 19.9, 14 and 13.5 at fasting, 1, 2, 3, and 4 h in the NoPoW versus 11.6, 15.3, 23.8, 21.8 and 16.3 in the DoPoW during the same duration. Plasma endotoxin activity had a significant positive correlation with menopause, but the activity was higher in the DoPoW than in the NoPoW [Table 2].
Table 2: Plasma endotoxin and LBP profile

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   Discussions Top

Metabolic diseases are associated with a low-grade inflammatory status. In our quest to determine a triggering factor of the early development of metabolic disease, we looked for a molecule involved early in the cascade of inflammation and identified LPS as a candidate. Furthermore, LPS stimulates release of several cytokines that are key inducers of insulin resistance. The concept of dietary excess is essentially linked to high-lipid intake induced inflammation. [27] LPS is a putative factor for the triggering of metabolic diseases. [28],[29] The mechanisms are allowing enteric LPS absorption are unclear but could be related to increased filtration of plasma LPS into lymph with fat absorption. [26]

Bacterial endotoxin is considered as a potential inflammatory mediator of atherosclerosis [2],[30],[31],[32] and has emerged as an independent predictor of atherosclerosis risk, [33] although the mechanisms for increased endotoxin in the plasma of some healthy individuals remain unknown. Chylomicrons promote intestinal absorption of LPS. More than 1 g of LPS can be found in the gut lumen. [34] Even small amounts of this highly proinflammatory substance could elicit strong inflammatory responses systemically, and hence, it is likely that the gut epithelium acts to effectively block the "translocation" of LPS and other microbial proinflammatory substances. However, small amounts of LPS are absorbed from the gut in healthy animals. [35] Excessive LPS absorption, however, could evidently be harmful and could lead to acute or chronic inflammation. Increased LPS absorption, for example, could exacerbate the risk for several chronic diseases, such as alcoholic liver injury. [36],[37] Hence, dietary fat could increase LPS absorption in several ways. One-way would be through promotion of the paracellular uptake of macromolecules as a result of deleterious effects of fatty acids (FA) on tight-junction integrity. An alternative mechanism explaining FA dependent LPS absorption may involve internalization of LPS by the enterocyte, followed by association of some of the internalized LPS with chylomicrons and concomitant basolateral secretion of LPS with the chylomicrons or by association of independently transcytosed LPS with newly released chylomicrons. Chylomicrons are associated with metabolic endotoxemia by promoting LPS absorption. [38],[39]

Lipoprotein lipase (LPL) activity was greater in diabetic postmenopausal women. The lower LPL activity in estrogen-sufficient women is consistent with other reports. [40],[41] Our finding that the association between LPL activity and meal FA storage was present in premenopausal, but not in postmenopausal women, suggests that the upregulated LPL activity in postmenopausal women is no longer rate-limiting for dietary FA storage, at least at this amount of dietary fat intake. Although some have found that postmenopausal women treated with estrogen increase fat oxidation, others have not observed differences in fat oxidation between postmenopausal women who were estrogen-deficient versus estrogen-sufficient. [42],[43] Our findings of reduced postprandial FA oxidation in postmenopausal women are consistent with the other previous reports. [44] Ovariectomized mice administered estrogen upregulate the skeletal muscle expression of peroxisome proliferator-activated receptor-d and peroxisome proliferator-activated receptor (PPAR)-α, [45],[46] which should increase fat oxidation. Hence future work must look at PPAR profiles in these patients. Latest evidence suggests, however that bacterial LPS derived from the gut microbiota may trigger inflammation and oxidative stress in response to diets. [47],[48],[49],[50],[51] High intake of fat or carbohydrates does not promote only endotoxemia, but also production of LPS transporting proteins and receptors. This "metabolic endotoxemia" has been shown to initiate or promote obesity, insulin resistance, metabolic syndrome, and finally diabetes. [47],[48],[49],[52]

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