Monocyte to high‐density lipoprotein cholesterol and lymphocyte to monocyte ratios are predictors of in‐hospital and long‐term mortality in patients with acute coronary syndrome
Muhammed OylumluMustafa OylumluBaran ArıkMuhammed DemirMehmet ÖzbekBayram ArslanBaris AcunNihat PolatMehmet Ata AkılMehmet Zihni Bilik
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Objective We aimed to determine the relationship between LMR and MHR and in-hospital and long-term mortality in patients with ACS. Methods We retrospectively collected patients with ACS undergoing coronary angiography between January 2012 and December 2013. Results In total, 825 patients with a mean age of 62.4 ± 12.9 years (71.3% male) were enrolled in the study. Patients were divided into three tertiles based on MHR levels and LMR levels. In-hospital mortality of the patients was significantly higher amongst patients in the upper MHR tertile when compared with the lower and middle MHR tertile groups [30 (10.9%) vs 8 (2.9%) and 14 (5.1%); P < .001, P = .009, respectively]. Five-year mortality of the patients was significantly higher amongst patients in the upper MHR tertile when compared with the lower and middle MHR tertile groups [84 (30.5%) vs 48 (17.5%) and 57 (20.7%); P < .001, P = .005, respectively]. In-hospital mortality of the patients was significantly higher amongst patients in the lower LMR tertile when compared with the upper and middle LMR tertile groups [25 (9.1%) vs 10 (3.6%) and 17 (6.2%); P = .007, P = .130, respectively]. Five -year mortality of the patients was significantly higher amongst patients in the lower LMR tertile when compared with the upper and middle LMR tertile groups [77 (28.0%) vs 47 (17.1%) and 65 (23.6%); P = .001, P = .142, respectively]. Conclusion We have shown that high MHR and low LMR were significant and independent predictors of in-hospital and long-term mortality in patients with ACS.Keywords:
Monocyte
This study was designed to compare the complete blood count values of opioid users (N = 61) and healthy subjects (N = 61), particularly monocyte-to-lymphocyte ratio (MLR) and platelet-to-lymphocyte ratio (PLR). PLR, MLR, and percentage of monocyte (MONO%) were significantly lower in opioid use disorder (OUD) group (P = 0.012, P = 0.005, P = 0.000). The area under the ROC curve of MLR and PLR levels for OUD was 0.349 and 0.368. MONO% correlated with substance use duration. Measurements like lymphocyte-related ratios and MONO% in opioid use can be important in substance monitoring, detection, and differentiation of acute and chronic conditions.
Monocyte
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Corticosterone (CORT) and other glucocorticoids cause peripheral insulin resistance and compensatory increases in β-cell mass. A prolonged high-fat diet (HFD) induces insulin resistance and impairs β-cell insulin secretion. This study examined islet adaptive capacity in rats treated with CORT and a HFD. Male Sprague-Dawley rats (age ∼6 weeks) were given exogenous CORT (400 mg/rat) or wax (placebo) implants and placed on a HFD (60% calories from fat) or standard diet (SD) for 2 weeks (N = 10 per group). CORT-HFD rats developed fasting hyperglycemia (>11 mM) and hyperinsulinemia (∼5-fold higher than controls) and were 15-fold more insulin resistant than placebo-SD rats by the end of ∼2 weeks (Homeostatic Model Assessment for Insulin Resistance [HOMA-IR] levels, 15.08 ± 1.64 vs 1.0 ± 0.12, P < .05). Pancreatic β-cell function, as measured by HOMA-β, was lower in the CORT-HFD group as compared to the CORT-SD group (1.64 ± 0.22 vs 3.72 ± 0.64, P < .001) as well as acute insulin response (0.25 ± 0.22 vs 1.68 ± 0.41, P < .05). Moreover, β- and α-cell mass were 2.6- and 1.6-fold higher, respectively, in CORT-HFD animals compared to controls (both P < .05). CORT treatment increased p-protein kinase C-α content in SD but not HFD-fed rats, suggesting that a HFD may lower insulin secretory capacity via impaired glucose sensing. Isolated islets from CORT-HFD animals secreted more insulin in both low and high glucose conditions; however, total insulin content was relatively depleted after glucose challenge. Thus, CORT and HFD, synergistically not independently, act to promote severe insulin resistance, which overwhelms islet adaptive capacity, thereby resulting in overt hyperglycemia.
Hyperinsulinemia
Corticosterone
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Aim: Our aim was to assess the effect of chronic hyperglycemia on glucose- and insulin-mediated suppression of glucagon secretion by the α-cell. Methods: Thirty subjects with normal glucose tolerance, 27 with impaired fasting glucose and/or impaired glucose tolerance, and 32 type 2 diabetic subjects were studied with oral glucose tolerance test (OGTT) and euglycemic hyperinsulinemic clamp. Fasting plasma glucagon concentration and plasma glucagon concentration during the OGTT and insulin clamp were measured. Results: During the OGTT, the decrement in the plasma glucagon concentration (area under the curve) was correlated inversely with the fasting plasma glucose concentration (r = −0.35; P < 0.001). As the fasting glucose level increased, the suppression of plasma glucagon progressively diminished. In contrast, during the euglycemic insulin clamp, the suppression of plasma glucagon was not correlated with the fasting plasma glucose concentration and was similar in subjects with normal glucose tolerance, subjects with impaired fasting glucose/impaired glucose tolerance, and diabetic subjects: 18, 23, and 18%, respectively. Conclusion: Insulin-mediated suppression of glucagon secretion is unrelated to the fasting plasma glucose concentration and is not impaired by chronic hyperglycemia. Thus, the defect in plasma glucagon suppression during the OGTT most likely results from impaired glucose-mediated glucagon suppression. The close correlation between fasting plasma glucose concentration and reduced glucagon suppression suggests a glucotoxic effect on α-cell function.
Glucose clamp technique
Glucose tolerance test
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The effect of 48 h of fasting in C57B1/6J-ob/ob and +/+ mice on body weight (BW), blood glucose (BG), serum immunreactive insulin (IRI), plasma immunoreactive glucagon (IRG) and on tissue levels of cyclic adenosine monophosphate (cAMP) were studied. Both groups of mice lost weight and demonstrated a decrease in BG and IRI with fasting. However, the BG and IRI of the ob/ob animals were initially highter and remained higher than those of the 2% of their initial weight while the +/+ lost 14 %. The +/+ mice exhibited an increase in cAMP levels in skeletal muscle, fat and liver with fasting, while the ob/ob mice had increased levels of cAMP in fat, but not in muscle. They also had a paradoxical decrease in liver cAMP levels with fasting, and associated with this was the lack of stimulation of glycogenolysis. Glycogenolysis was significant in the livers of fasted +/+ mice. The plasma IRG levels of the fed ob/ob mice were significantly higher (1.8) times) than those of the fed +/+ mice. Islet cAMP levels were decreased with fasting in ob/ob mice. However, the levels were significantly higher in 48-h faster ob/ob mice compared to the fasted +/+ group. The apparent paradoxical response to fasting observed in the livers of the ob/ob mice remains unexplained.
Glycogenolysis
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Abstract Dysregulation of the adipoinsular axis in male obese Zucker diabetic fatty (ZDF; fa/fa) rats, a model of type 2 diabetes, results in chronic hyperinsulinemia and increased de novo lipogenesis in islets, leading to β-cell failure and diabetes. Diazoxide (DZ; 150 mg/kg·d), an inhibitor of insulin secretion, was administered to prediabetic ZDF animals for 8 wk as a strategy for prevention of diabetes. DZ reduced food intake (P < 0.02) and rate of weight gain only in ZDF rats (P < 0.01). Plasma insulin response to glucose load was attenuated in DZ-Zucker lean rats (ZL; P < 0.01), whereas DZ-ZDF had higher insulin response to glucose than controls (P < 0.001). DZ improved hemoglobin A1c (P < 0.001) and glucose tolerance in ZDF (P < 0.001), but deteriorated hemoglobin A1c in ZL rats (P < 0.02) despite normal tolerance in the fasted state. DZ lowered plasma leptin (P < 0.001), free fatty acid, and triglyceride (P < 0.001) levels, but increased adiponectin levels (P < 0.02) only in ZDF rats. DZ enhanced β3-adrenoreceptor mRNA (P < 0.005) and adenylate cyclase activity (P < 0.01) in adipose tissue from ZDF rats only, whereas it enhanced islet β3- adrenergic receptor mRNA (P < 0.005) but paradoxically decreased islet adenylate cyclase activity (P < 0.005) in these animals. Islet fatty acid synthase mRNA (P < 0.03), acyl coenzyme A carboxylase mRNA (P < 0.01), uncoupling protein-2 mRNA (P < 0.01), and triglyceride content (P < 0.005) were only decreased in DZ-ZDF rats, whereas islet insulin mRNA and insulin content were increased in DZ-ZDF (P < 0.01) and DZ-ZL rats (P < 0.03). DZ-induced β-cell rest improved the lipid profile, enhanced the metabolic efficiency of insulin, and prevented β-cell dysfunction and diabetes in diabetes-prone animals. This therapeutic strategy may be beneficial in preventing β-cell failure and progression to diabetes in humans.
Hyperinsulinemia
Lipogenesis
Diazoxide
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배경: 인듐은 휴대전화, TV를 비롯한 디지털기기에서 디스플레이패널의 핵심소재로 사용되는 금속이다. 과거 인듐은 인체에 무해한 금속으로 여겨졌으나 인듐노출로 인한 폐질환자와 사망자 발생을 계기로 일부 국가에서 그 유해성에 대한 연구가 진행되고 있다. 우리나라는 디스플레이 패널 세계시장점유율 1위로 세계 디스플레이 패널의 약 50%를 공급하고 있는 세계 제1의 인듐 소비 국가이다. 하지만 인듐 노출에 의한 건강영향 연구는 미비한 상황이며 폐질환 예방체계 및 검진기준 또한 마련되지 못한 실정이다. 따라서 본 연구를 통해 국내 인듐취급 근로자를 대상으로 백혈구 수치 변화를 확인하고 검진기준 마련을 위한 기초자료를 제공하고자 하였다. 방법: 국내에서 인듐을 취급하는 디스플레이 제조 관련 공장의 남성근로자 156명을 대상으로 하였다. 혈청 인듐은 ICP-MS (bruker), KL-6는 ELISA (EIDIA), 백혈구 분별계수는 자동혈구계수기(sysmex XE-2100)를 이용하여 분석하였다. 자료분석은 version18.0 SPSS Statistics 프로그램을 이용하였고 통계적 유의수준은 p＜0.05로 하였다. 결과: 혈청인듐의 일본참고치 3 μg/L 초과자에서 neutrophil, lymphocyte, monocyte, eosinophil이 의미있는 변화를 보였으며 인듐농도의 증가에 따라 neutrophil의 증가경향과 lymphocyte의 감소경향이 뚜렷하였다(p for trend＜0.05). KL-6의 일본참고치 500 U/mL 초과자에서는 neutrophil, lymphocyte, monocyte의 변화가 의미 있었으며 KL-6의 농도 증가에 따라 neutrophil은 증가하였으나, lymphocyte, monocyte, eosinophil은 뚜렷한 감소경향을 보였다(p for trend＜0.05). 혈청 인듐 또는 KL-6를 독립변수로, 백혈구 분별계수 결과 및 백분율을 독립변수로 회귀분석을 실시한 결과 혈청인듐은 영향력이 낮았으나 KL-6는 neutrophil의 증가와 lymphocyte, monocyte의 감소에 영향을 주는 것으로 분석되었다. 결론: 백혈구 총 수치와 분별계수결과는 모두 정상범위이나 일본의 참고치를 초과한 그룹에서 neutrophils의 증가, lymphocyte와 monocyte의 의미 있는 감소가 확인되었다. 이는 연구대상자에서 neutrophil을 증가시킬 수 있는 감염, 스테로이드 약물치료 등이 없었으며 혈청 인듐 농도 및 간질성폐질환의 마커인 KL-6의 농도 변화에 따라 의미 있는 변화를 보였으므로 직업적 인듐노출로 인한 백혈구 수치의 변화라고 판단된다. 고농도의 인듐노출에서도 변화의 폭이 작아 진단지표로 활용가치는 낮으나 특발성폐섬유증, 폐석면증 등의 질환에서 neutrophil이 증가하였다는 보고가 있으므로 인듐에 의한 간질성 폐질환예방을 염두에 둔 진단항목 개발과 인듐에 의한 폐질환발생기전 파악 등의 후속연구 진행이 요구된다.
Monocyte
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The effect of sera from patients with Hodgkin's disease (HD) on monocyte dependent ConA and MLC-activation of normal lymphocytes to DNA synthesis was studied. Lymphocyte stimulation was greatly enhanced in the presence of monocytes at a monocyte : lymphocyte ratio of less than or equal to 8 : 1. Higher ratios were usually suppressive. Some HD sera suppressed monocyte mediated enhancement of ConA and MLC-stimulation efficiently. The degree of inhibition by the individual HD serum remained similar in the absence of monocytes and at various monocyte : lymphocyte ratios. Pretreatment of monocytes or lymphocytes with HD serum had no effect. Inhibition was only noted when serum was present during the whole culture period. It is concluded that HD sera do not hamper the activity of monocytes to augment lymphocyte growth. The effect may be explained by direct effects of serum factors on lymphocytes.
Monocyte
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In normal rats, females have higher circulating GH-binding protein (GHBP) levels than males, whereas in the GH-deficient dwarf (Dw) rat, there is no sexual dimorphism in plasma GHBP, suggesting that GH secretion may be involved in this difference. In order to study the relationship between gonadal steroids and GH on GHBP and GH receptor regulation, the levels of plasma GHBP, hepatic bovine GH, and human GH (hGH) binding as well as GHBP and GH receptor messenger RNA (mRNA) have now been studied in normal, Dw, hypophysectomized (Hx), or ovariectomized (Ovx) rats, subjected to different GH and gonadal steroid exposure. In normal male rats, estradiol (E2, 12.5-25 micrograms/day for 1 or 2 weeks) markedly increased plasma GHBP and hepatic hGH, and bGH binding. These effects of E2 were diminished in Dw rats, absent in Hx rats, but restored in Hx rats given exogenous hGH. Plasma GHBP rose in female rats given E2, and fell in females given the anti-estrogen tamoxifen. Ovx animals had lower plasma GHBP and hepatic GH binding which was reversed by E2, but not testosterone treatment. Continuous hGH infusions in Ovx rats restored hepatic GH binding, and increased plasma GHBP. In Dw males, hGH increased plasma GHBP and hepatic GH binding, whereas testosterone had no effect on GHBP or GH receptors and did not affect their up-regulation by hGH. Hepatic levels of GHBP-, and GH receptor mRNA transcripts showed the same trends in response to steroid or GH treatment, but the differences were rarely significant, except in Ovx animals which had higher GHBP mRNA transcripts after GH or E2 treatment. Thus E2 and GH increase both plasma GHBP and hepatic GH receptor binding. GH up-regulates GHBP in the absence of E2, whereas E2 treatment does not raise GHBP in the absence of GH. Whereas some of the effects of estrogen could be mediated via alterations in GH secretion, estrogen may also directly influence GHBP production at the liver, but only in the presence of GH.
Growth hormone-binding protein
Sexual dimorphism
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Plasma glucose, insulin, and FFA concentrations were determined in 15 normal subjects and 15 patients with noninsulin-dependent diabetes mellitus (NIDDM) from 0800 to 1600 h. Breakfast and lunch were consumed at 0800 and 1200 h, respectively, and plasma concentrations were measured at hourly intervals from 0800-1600 h. Plasma glucose concentrations between 0800 and 1600 h were significantly elevated in patients with NIDDM, and the higher the fasting glucose level, the greater the postprandial hyperglycemia. Hyperglycemia in patients with NIDDM was associated with plasma insulin levels that were significantly higher (P less than 0.001) than those in normal subjects, and substantial hyperinsulinemia occurred between 0800 and 1600 h in patients with mild NIDDM (fasting plasma glucose concentrations, less than 140 mg/dl). Both fasting and postprandial FFA levels were also increased in patients with NIDDM (P less than 0.001), and the greater the plasma glucose response, the higher the FFA response (r = 0.70; P less than 0.001). However, there was no significant correlation between plasma insulin and FFA concentrations. More specifically, hyperinsulinemic patients with mild diabetes (fasting plasma glucose, less than 140 mg/dl) maintained normal ambient FFA levels, while FFA concentrations were significantly elevated in patients with severe NIDDM (fasting plasma glucose, greater than 250 mg/dl), with insulin concentrations comparable to those in normal subjects. These results demonstrate that patients with NIDDM are not capable of maintaining normal plasma FFA concentrations. This defect in FFA metabolism is proportionate to the magnitude of hyperglycemia and occurs despite the presence of elevated levels of plasma insulin. These results are consistent with the view that insulin resistance in NIDDM also involves the ability of insulin to regulate FFA metabolism.
Hyperinsulinemia
Carbohydrate Metabolism
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Insulin and glucagon secretion was compared in women with impaired glucose tolerance (IGT; n = 19, age 58.4 +/- 0.3 yr; mean +/- SD) and women with normal glucose tolerance (NGT; n = 40, age 58.4 +/- 0.3 yr). Fasting plasma insulin levels were higher in IGT than in NGT (P = 0.026), whereas fasting glucose and glucagon levels were not different. Arginine was injected intravenously (5 g), which rapidly stimulated insulin and glucagon secretion in all subjects. Raising the blood glucose (BG) to 14 and 28 mmol/L potentiated insulin secretion and inhibited glucagon secretion. The acute insulin response to arginine (AIR = 2-5 min postload increase) at BG 14 mmol/L, but not at fasting BG or BG 28 mmol/L, was lower in IGT than in NGT (P = 0.033), as was the glucose potentiation of AIR (slopeAIR) (P = 0.020). The acute glucagon response (AGR) was higher in IGT than in NGT at BG 14 mmol/L (P = 0.016). SlopeAGR (glucose inhibition of AGR) was reduced in IGT (P = 0.001). In NGT, there was a significant inverse correlation between slopeAIR and slopeAGR (P = 0.002) not seen in IGT. We conclude that in IGT with normal fasting BG, the glucose modulation of islet function is impaired, indicating that islet dysfunction is an early lesion during the development of noninsulin-dependent diabetes mellitus.
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