Plasma Leptin Levels In Patients Research Articles

Increased plasma leptin as a novel predictor for psychopathological depressive symptoms in chronic schizophrenia

BackgroundDepressive symptoms are often seen in schizophrenia. The overlap in presentation makes it difficult to distinguish depressive symptoms from the negative symptoms of schizophrenia. The adipokine leptin was found to...

Relationship between plasma leptin levels and clinical outcomes of pediatric traumatic brain injury

High plasma leptin level has been associated with mortality after adult intracerebral hemorrhage. The present study was undertaken to investigate the plasma leptin concentrations in children with traumatic brain injury and to analyze the correlation of leptin with pediatric traumatic brain injury outcome. Plasma leptin concentration of eighty-nine healthy children and 142 children with acute severe traumatic brain injury was measured by enzyme-linked immunosorbent assay. Twenty-six patients (18.3%) died and 42 patients (29.6%) had an unfavorable outcome (Glasgow outcome scale score of 1–3) at 6 months after traumatic brain injury. Upon admission, plasma leptin level in patients was substantially higher than that in healthy controls. A forward stepwise logistic regression selected plasma leptin level as an independent predictor for 6-month mortality and unfavorable outcome of patients. A receiver operating characteristic curve analysis showed plasma leptin level better predicted 6-month mortality and unfavorable outcome. The prognostic value of leptin was similar to that of Glasgow Coma scale score for 6-month clinical outcomes. Thus, plasma leptin level represents a novel biomarker for predicting 6-month clinical outcome in children with traumatic brain injury.

The effect of short-term exercise on plasma leptin levels in patients with anorexia nervosa

Plasma leptin concentrations are markedly reduced in malnourished patients with anorexia nervosa (AN). Whether the long-term underweight and low-fat stores affect the leptin response to exercise remains unknown. We investigated the effect of 45-minute cycle ergometer exercise (2 W kg −1 of lean body mass [LBM]) on plasma leptin, norepinephrine (NE), glycerol, and insulin levels in 10 patients with AN and in 15 healthy age-matched women (C). Plasma leptin levels immediately and 90 minutes after the exercise bout were significantly reduced compared with basal leptin levels in both AN and C groups ( P < .05). Compared with the control trial, leptin levels were significantly lower immediately and 90 minutes after exercise in the AN group ( P < .05) but not in the C group. Basal and exercise-induced plasma glycerol and NE levels did not differ significantly between the groups. Basal and exercise-induced plasma insulin levels were significantly lower in the AN group compared with the C group ( P < .05). In conclusion, we demonstrated that a single bout of low-intensity exercise significantly reduces plasma leptin levels in patients with AN. In healthy women, exercise had no effect on lowering leptin concentrations beyond the diurnal decrease that occurs in the absence of exercise. Neither NE nor insulin are responsible for the different response of leptin to exercise in AN.

Plasma Leptin Levels in Patients with Floppy Eyelid Syndrome

To determine the range of plasma leptin levels in patients with floppy eyelid syndrome (FES). This was a retrospective, noninterventional case series of 11 patients with FES. Charts were reviewed for patient age, sex, plasma leptin level, body mass index (BMI), presence or absence of obstructive sleep apnea (OSA) and diabetes mellitus, and any treatments for OSA. Charts of 11 patients were reviewed (10 male, 1 female). Plasma leptin levels were elevated in 7 of 11 patients (64%). Mean plasma leptin concentration was 49.5 ng/ml in male patients (range, 5 to 120 ng/ml) compared with a normal range of 1 to 35 ng/ml. Plasma leptin level in the female patient was 180 ng/ml (normal range, 4 to 72 ng/ml). Five patients had a known diagnosis of OSA. Four of these patients received continuous positive airway pressure during leptin level measurement. Plasma leptin levels averaged 110.0 ng/ml in the continuous positive airway pressure group. Average BMI was 37.4 kg/m (range, 24.9 to 57.1 kg/m). All patients with elevated leptin levels had a high BMI. Patients with FES demonstrate elevated plasma leptin levels, which correlate with BMI. Hyperleptinemia may play a role in the pathogenesis of FES.

In addition to reducing BP, moxonidine improves insulin resistance and reduces plasma leptin levels in patients with obesity and hypertension,

In addition to reducing BP, moxonidine improves insulin resistance and reduces plasma leptin levels in patients with obesity and hypertension,

Leptin concentrations in the abdominal subcutaneous adipose tissue of patients with anorexia nervosa assessed by in vivo microdialysis

Objective The adipocyte-derived hormone leptin is involved in energy metabolism and body weight regulation. Plasma leptin concentrations are significantly reduced in patients with anorexia nervosa (AN) and with severe malnutrition. Whether reduced plasma leptin is reflected by its decreased production by the adipose tissue is unknown. Methods In the present study we measured leptin concentrations locally in the abdominal subcutaneous adipose tissue of 9 female AN patients and 11 healthy controls by in vivo microdialysis. Results Adipose tissue free leptin levels were not different in patients with AN compared to controls (2.59±1.99 vs 2.36±0.25 ng/ml, P>0.05). Plasma leptin soluble receptor (sOb-R) levels were significantly higher in patients with AN than in healthy subjects (58.05±38.69 vs 12.79±5.08 U/ml, P<0.01). The area of adipocyte in AN was considerably smaller than in the controls (183±104.01 μm 2 compared to 2145.8±1003.41). Conclusions We conclude that decreased plasma leptin levels in patients with AN are not directly related to dialysate leptin levels in the abdominal subcutaneous adipose tissue.

Plasma leptin concentration in patients with acute renal failure.

Acute renal failure (ARF) is characterized by impaired excretory, endocrine, homeostatic and metabolic function of the kidneys. It is well-known that leptin is an adipose-derived polypeptide hormone which is predominantly biodegraded by the kidneys. Therefore, plasma leptin concentration is increased in chronic renal failure (CRF). However, its' concentrations in patients with ARF were not investigated until now. The aim of the present study was to evaluate plasma leptin concentration in patients with ARF. 27 patients with ARF (age 44 +/- 4 years, BMI 26.0 +/- 0.9 kg/m2, means +/- SEM, 17 patients 15 M, 2 F recovered kidney function and 10 patients 7 M, 3 F died during the anuric phase), 27 hemodialysis patients (22 M, 5 F; age 45 +/- 2 years; BMI 26.2 +/- 0.8 kg/m2) with chronic renal failure (CRF) and 27 healthy subjects (HS) (22 M, 5 F; age 42 +/- 3 years; BMI 25.9 +/- 0.6 kg/m2) were examined. In patients with ARF, blood samples for plasma leptin and routinely assessed biochemical parameters were withdrawn before the first HD session (I), and in patients who survived a second time 5 days later during the anuric/oliguric phase (II), and a third one during the polyuric phase before discharge of the patient from hospital (III). In patients with CRF all examined parameters were estimated only once before a subsequent HD session. Patients with ARF (before the first HD session) and CRF did not differ significantly with respect to BMI, serum creatinine and blood hydrogen ion concentrations. Plasma leptin level in patients with ARF before the first HD session was similar to values obtained in HS, but significantly lower (p < 0.01) than in patients with CRF (2.5 (1.9 - 8.2) vs. 3.4 (2.5 - 8.3) vs. 8.4 (2.9 - 16.9) ng/ml in ARF, HS and CRF, respectively). There was no significant difference in leptinemia between patients with ARF who survived and who died. In patients with ARF who survived, improvement ofrenal function was accompanied by a slightly (not significant) declining tendency in plasma leptin concentration (5.6 +/- 2.2 vs. 4.8 +/- 1.7 vs. 4.5 +/- 1.3 ng/ml; I, II, III phases of ARF, respectively). In contrast to hemodialysis patients with chronic renal failure, patients with acute renal failure are characterized by normal plasma leptin concentration. Thus, difference in leptinemia between patients with chronic and acute renal failure seems to be due to preservation of large amounts of active renal parenchyma in ARF patients.

Concentraciones plasmáticas de leptina en los pacientes con cirrosis biliar primaria y su relación con el grado de fibrosis

a) To analyze plasma leptin levels in patients with primary biliary cirrhosis (PBC) and b) to investigate the relationship between leptin levels and liver fibrosis stage in a cohort of patients with PBC. Serum leptin levels were evaluated through radioimmunoassay in 30 patients with PBC (mean age: 37.2 +/- 11.0 years; range:19-75) and in 29 controls matched for age and weight. Venous blood obtained after a 12-hour fast was centrifuged in EDTA tubes. Weight, height and body mass index (BMI) were measured using standard methods. Hepatitis C virus RNA was determined using qualitative and quantitative polymerase chain reaction. In all patients liver biopsies were performed and the degree of fibrosis and extent of inflammatory infiltrate were evaluated. Plasma leptin levels in patients with PBC were lower than those obtained in control subjects (p<0.0001). No significant differences were found between the two groups in age, weight, height, BMI or body fat index. There was a clear increase in serum leptin levels according to histological stage of PBC (stage I: 2.1 ng/ml; stage II: 4.3 ng/ml; stage III: 5.3 ng/ml; stage IV: 12.1 ng/ml; p<0.01) The present study demonstrates the correlation between leptin and stage of liver fibrosis in a cohort of patients with PBC, providing further evidence of the involvement of leptin in the process of liver fibrosis.

Comparative Analysis of Plasma Leptin Levels in Both Genders of Patients with Essential Hypertension and Healthy Subjects

While pathogenesis of hypertension is not clearly deciphered yet, increase in body weight, most of the time, is associated with hypertension. There are reports indicating that leptin, product of the Ob gene mainly synhesized in adipocytes, may have role(s) in hypertension, but contribution of the gender is rather contradictive. In the present study, plasma leptin levels in patients of both genders with hypertension and normotensive controls were measured and the relationship between plasma leptin levels and BMI were evaluated in both sexes. Total of 62 patients (31 M/31 F) diagnosed with essential hypertension who were not under any anti‐hypertensive medication were admitted into the study. The control group was composed of 56 (25 M/31 F) age‐, BMI‐ and sex‐matched healthy normotensive volunteers. Plasma leptin levels were determined by a commercial ELISA kit. Plasma leptin and leptin/BMI levels (Mean ± SEM) of women (n:62) were significantly higher than men (n:56) (20.10 ± 1.47 ng/ml versus 4.72 ± 0.50 ng/ml; p < 0.0001). Plasma leptin and leptin/BMI levels of patients of both genders with hypertension were significantly higher than in normotensive subjects (p < 0.05). Leptin and leptin/BMI levels in obese hypertensives were higher than obese normotensives (p < 0.05). Obese hypertensive women had higher leptin and leptin/BMI levels than obese normotensive women (p < 0.05). In conclusion, these results support the hypothesis that a possible link exists between leptin and hypertension. Further studies are needed to clarify how increased levels of leptin affects the pathophysiology of hypertension.

Plasma leptin levels in patients with burn injury: a preliminary report

The purpose of this study was to investigate the relationship between the plasma leptin level and clinical parameters in patients with burn injury. Six patients with burn injury were admitted to the Emergency and Critical Care Medicine Center of St. Marianna University Hospital within 1 h after injury. Plasma levels were monitored for leptin, proinflammatory cytokines (interleukin (IL)-1β, IL-6, tumor necrosis factor α (TNF α)), stress-related parameters (adrenocorticotropic hormone (ACTH), cortisol, and C-reactive protein (CRP)). The change in individual plasma leptin levels did not show similar pattern in all these patients. However, leptin levels remained within the normal range, except in a patient (Case 1) complicated with severe hypovolemic shock. Plasma ACTH and cortisol levels were also elevated in most of the patients. Examination of relationships among plasma leptin, proinflammatory cytokines, and stress-related parameters revealed a significant positive correlation between the plasma leptin level and IL-1β or IL-6. These results suggest that the plasma leptin level may have some relations to plasma proimflammatory cytokines in pathophysiologic responses to critical conditions of burn injury.

The effect of therapeutically induced weight gain on plasma leptin levels in patients with anorexia nervosa

Previously it was shown that hyperleptinemia ensues from the therapeutically induced weight gain in patients with anorexia nervosa (AN). However, not all studies have been able to confirm this finding. To further investigate leptin secretion during weight gain in AN and potential functional implications serum leptin levels, body mass index (BMI),% body fat, fT3, fT4 and TSH of 18 adolescent AN patients (BMI at admission: 14.4±1.2) were examined four times during 11 weeks of re-feeding and compared to 18 weight stable controls. Additionally, serum leptin levels, BMI and % body fat were determined in patients reaching target weight after 11–20 weeks (mean 14.3±3) of inpatient re-feeding. At admission patients showed lower lg10 leptin levels ( P=0.000) and BMI ( P=0.000) than controls. At target weight patients still had significantly lower BMI ( P=0.000) and% body fat ( P=0.000) than controls but lg10 leptin levels of patients were higher than those of controls when adjusted for BMI and% body fat (ANCOVA, group P=0.038). In patients, correlation coefficients between lg10 leptin levels and BMI increments increased during the 11 weeks of re-feeding. BMI,% body fat and fT3 levels were not significantly correlated to lg10 leptin levels in week 11, however, 53% of the variance of leptin levels (corrected R 2=0.53, P=0.001) was explained by BMI increments between weeks 7 and 11 ( P=0.001) and lg10 leptin level at admission ( P=0.002). In conclusion, we confirmed weight gain induced hyperleptinemia in AN. Further research is required to assess if this phenomenon contributes to renewed weight loss.

Plasma leptin levels and cardiac sympathetic function in patients with obstructive sleep apnoea-hypopnoea syndrome

Background: The control of body weight and cardiac sympathetic function in patients with obstructive sleep apnoea-hypopnoea syndrome (OSAHS) are important because both factors have significant effects on the mortality of...

Low Leptin Levels but Norma Body Mass Indices in Patients with Depression or Schizophrenia

Appetite, food intake and weight are frequently altered in psychiatric disorders such as major depression and schizophrenia. The few studies investigating weight and the body mass index (BMI) have yielded variable results. Leptin, a fat cell-derived hormone signalling to the brain the size of the adipose tissue, plays a pivotal role in the regulation of weight and food intake. Moreover, leptin is involved in the control of other behaviors and in brain development. There is almost no information about the amounts of circulating leptin in major depression or schizophrenia. We investigated the BMI and plasma leptin levels in patients with major depression (n = 62), schizophrenia (n = 42), and in healthy controls (n = 64). Mean BMIs did not differ between groups. However, leptin levels were significantly lower in both patient groups compared to healthy controls. Moreover, patients suffering from schizophrenia showed significantly lower leptin levels than depressed patients. Decreased leptin levels were independent of psychotropic medication. We conclude that depression and schizophrenia go along with decreased systemic leptin concentrations that cannot be explained by medication or an altered BMI. Hence, leptin might play an important pathophysiological role in these psychiatric disorders that deserves further scientific attention.

Insulin regulation of leptin synthesis and secretion in humans: the model of myotonic dystrophy.

Myotonic dystrophy (MyD) is a systemic disorder in which insulin resistance is well recognized. In the present study we have characterized plasma leptin levels in patients with MyD and in age, sex and body mass index (BMI) matched controls and assessed the influence of leptin on the clinical manifestations of MyD. Body composition, plasma leptin, fasting and post-oral glucose tolerance test insulin, IGF-I and IGFBP3 were studied in 34 MyD patients and 33 controls. Body composition was measured using a bioelectrical impedance analyzer, and circulating levels of insulin, leptin, IGF-I, IGFBP3 were measured by IRMA or RIA. Insulin sensitivity was modelled according to a homeostasis model assessment (HOMA) computer-solved model. Percentage body fat was higher in patients than in controls (25.6 +/- 2.28% vs 18.8 +/- 1.53%, P = 0.013). Insulin levels, both fasting and after oral glucose were higher in patients than in controls, and insulin sensitivity was lower in patients than in controls. Serum leptin was higher in patients than in controls (20.98 +/- 3.11 micrograms/l vs 10.4 +/- 1.31 micrograms/l, P = 0.004), and higher in women than in men, both in patients and in controls. In patients, leptin levels were correlated with age, BMI, fasting insulin, insulin area under curve and lower insulin sensitivity, whereas leptin levels were not correlated with body fat or other parameters of body composition. In controls, leptin levels were correlated with BMI and body fat. The results were evaluated using logistic regression models for each of the 2 populations. In the model of MyD, insulin resistance and age correctly identified higher leptin levels in relation to controls out of 87.88% of patients, and in the model of controls male sex with a negative correlation and BMI correctly identified their leptin levels out of 84.33% cases. These findings show that MyD provides a different model of leptin regulation in humans, and suggest that in MyD patients there are correlations between leptin and insulin resistance and age, irrespective of body fat. In contrast, leptin levels in controls, correlate with sex and BMI. The data on leptin in this population of patients can not be related aetiologically to the muscle disease itself.

Circadian Plasma Leptin Levels in Patients with Anorexia nervosa: Relation to Insulin and Cortisol

In anorexia nervosa, underweight results from a loss of body mass due to a restricted energy intake. Circulating leptin levels have been shown to be low in the acute stage of the disorder. We studied diurnal secretion characteristics of leptin, insulin and cortisol in a study group of anorectic patients prior to refeeding, a second study group of anorectic patients after initiation of refeeding and study groups of healthy underweight and normal-weight controls. Spontaneous secretion of leptin, insulin and cortisol was measured by drawing blood samples every 2 h for 24 h. The temporal relationships between the diurnal secretion patterns of the three hormones were assessed by cross-correlation analysis in every study group. Plasma levels of leptin and cortisol were secreted with a specific circadian rhythmicity and displayed an intricate temporal relationship in anorectic patients. Semistarvation in the non-refed patients was associated with (1) exceedingly low plasma leptin levels, (2) a qualitative alteration in the circadian rhythm of leptin and cortisol levels and (3) an alteration in the temporal coupling between cortisol and leptin. In contrast, in the patients who had gained weight, leptin levels were higher; furthermore, the diurnal pattern of leptin and the temporal relationship between leptin and cortisol were similar to controls. Increments in insulin secretion preceded those of leptin by 4–6 h in both anorectic patients and in controls. Leptin levels increased 4 h prior to those of cortisol in controls and in refed patients, whereas in the non-refed patients cortisol increased prior to leptin. Thus, anorexia nervosa leads to pronounced, albeit reversible changes in the secretion dynamics of leptin and cortisol.

G004 Plasma leptin levels in patients with essential hypertension - modulatory effects of maximal and submaximal exercise

G004 Plasma leptin levels in patients with essential hypertension - modulatory effects of maximal and submaximal exercise

Glucocorticoid regulation of leptin synthesis and secretion in humans: elevated plasma leptin levels in Cushing's syndrome.

Leptin, the obese (ob) gene product, is an adipocyte-derived satiety factor that is involved in the regulation of food ingestion and body weight. To investigate glucocorticoid regulation of leptin synthesis and secretion in humans, we measured plasma leptin levels in patients with Cushing's syndrome with adrenal or pituitary adenoma and in patients with iatrogenic Cushing's syndrome. Plasma leptin levels in patients with Cushing's syndrome were significantly elevated compared to those in nonobese healthy subjects and obese subjects without any metabolic or endocrine diseases at a given percentage of body fat by analysis of covariance. In patients with adrenal or pituitary adenoma, after the tumor resection, plasma leptin levels were reduced, with a concurrent decrease in plasma cortisol levels. With no significant changes in body weight, plasma leptin levels were also elevated significantly in lean healthy volunteers 24 h after the administration of 1 mg dexamethasone. Dexamethasone potently induced ob gene expression and leptin secretion in the organ culture of human adipose tissue. The data demonstrate that glucocorticoids act, at least in part, directly on the adipose tissue and increase leptin synthesis and secretion in humans.

Plasma leptin levels do not change in patients with Cushing's disease shortly after correction of hypercortisolism.

In the present study, we characterized the changes in plasma leptin levels in patients with pituitary Cushing's disease and in age- and sex-matched controls. Plasma levels of ACTH, cortisol, and leptin were measured before and after iv administration of ovine CRH in controls once and in patients twice (while they had active hypercortisolism and 10 days after successful surgery). Cushing's patients had elevated body mass indexes (34 +/- 1.9 vs. 22.9 +/- 0.8) and plasma leptin levels (35.6 +/- 3.4 vs. 9.2 +/- 1.9 ng/mL) compared to controls, which remained unchanged 10 days after successful transsphenoidal surgery and directly proportional to the body mass index. Plasma leptin levels were not affected by CRH infusion in either the controls or the patients despite clear-cut elevations in plasma ACTH and cortisol. These findings suggest that although acute changes in plasma cortisol do not affect plasma leptin, chronic hypercortisolism results in elevated leptin levels, probably by causing visceral obesity.

Renal function and insulin resistance as determinants of plasma leptin levels in patients with NIDDM

Plasma leptin level is known to correlate with the degree of obesity. To determine the influences of renal function and insulin resistance on plasma leptin concentrations, we measured plasma leptin concentrations and performed the euglycaemic hyperinsulinaemic clamp studies in 57 patients with non-insulin-dependent diabetes mellitus with a wide range of renal function. In simple regression analyses, plasma leptin concentration showed significant positive correlations with percentage of body fat measured by dual energy X-ray absorptiometry, body mass index, waist to hip ratio and fasting plasma insulin. Leptin level was higher in females than males. Multiple regression analyses indicated that percent body fat, waist to hip ratio, plasma insulin, gender and renal function (1/creatinine), but not insulin sensitivity, were significant and independent determinants of plasma leptin level. These results suggest that plasma leptin level is regulated or affected by multiple factors including renal function. Insulin resistance appeared to increase leptin levels indirectly by raising plasma insulin.