Nocturnal rise of leptin in lean, obese, and non-insulin-dependent diabetes mellitus subjects.

Sinha, Madhur K.; Ohannesian, Joanna P.; Heiman, Mark L.; Kriauciunas, Aidas; Stephens, T.; Magosin, Susan; Marco, Cheryl; F, J

doi:10.1172/jci118551

Cited by 721 publications

(504 citation statements)

References 27 publications

(21 reference statements)

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“…Thus, the CSF:plasma leptin ratio is lower in girls, and this may underlie the propensity towards excess body fat [33]. A nocturnal plasma leptin surge entrained to meal timing has been demonstrated in lean and obese humans [34,35]. However, this is not accompanied by an increase in CSF leptin [36].…”

Section: Discussionmentioning

confidence: 99%

Adiponectin complexes in human cerebrospinal fluid: distinct complex distribution from serum

et al. 2007

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Aims/hypothesis Adiponectin is an adipocyte-derived secretory factor that is specifically produced in adipocytes. It exerts effects on energy homeostasis via peripheral and central mechanisms. However, it is not clear whether adiponectin crosses the blood-brain barrier in humans. In serum, adiponectin circulates in several different complexes, each of which has distinct functions. Here, we wanted to test whether adiponectin can be found in human cerebrospinal fluid (CSF) and whether specific adiponectin complexes are enriched in CSF compared with peripheral serum samples. We also wanted to establish whether there is a sex-related difference with regard to the distribution of adiponectin oligomers in CSF. Materials and methods We studied 22 subjects (11 men, 11 women) in this study. Their average BMI was 28.0± 4.7 kg/m 2 ; average age was 70±7 years. Results Analysis of total adiponectin revealed that adiponectin protein is present in human CSF at approximately 0.1% of serum concentration. The distribution of adiponectin oligomers differs considerably in CSF from that of serum within matched samples from the same patients. Only the adiponectin trimeric and low-molecular-mass hexameric complexes are found in CSF, with a bias towards the trimeric form in most patients. Male subjects have a higher CSF: serum ratio of total adiponectin (p<0.05; n=20) and have slightly higher trimer levels in serum and CSF than female subjects. Conclusions/interpretation We conclude that the adiponectin trimer is the predominant oligomer in human CSF.

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Section: Discussionmentioning

confidence: 99%

Adiponectin complexes in human cerebrospinal fluid: distinct complex distribution from serum

et al. 2007

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“…The plasma leptin level is known to vary somewhat throughout the day (46,47), and, apparently, the amplitude of the diurnal variations is influenced by factors, such as diet composition, physical activity, insulin levels, and energy balance (46,48,49). Therefore, fasting leptin concentration may not reflect the mean leptin concentration during the day.…”

Section: Discussionmentioning

confidence: 99%

Leptin Levels Are Associated with Fat Oxidation and Dietary‐Induced Weight Loss in Obesity

et al. 2001

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Objective: To examine the relationship between fasting plasma leptin and 24-hour energy expenditure (EE), substrate oxidation, and spontaneous physical activity (SPA) in obese subjects before and after a major weight reduction compared with normal weight controls. To test fasting plasma leptin, substrate oxidations, and SPA as predictive markers of success during a standardized weight loss intervention. Research Methods and Procedures: Twenty-one nondiabetic obese (body mass index: 33.9 to 43.8 kg/m 2 ) and 13 lean (body mass index: 20.4 to 24.7 kg/m 2 ) men matched for age and height were included in the study. All obese subjects were reexamined after a mean weight loss of 19.2 kg (95% confidence interval: 15.1-23.4 kg) achieved by 16 weeks of dietary intervention followed by 8 weeks of weight stability. Twenty-four-hour EE and substrate oxidations were measured by whole-body indirect calorimetry. SPA was assessed by microwave radar. Results: In lean subjects, leptin adjusted for fat mass (FM) was correlated to 24-hour EE before (r ϭ Ϫ0.56, p Ͻ 0.05) but not after adjustment for fat free mass. In obese subjects, leptin correlated inversely with 24-hour and resting nonprotein respiratory quotient (r ϭ Ϫ0.47, p Ͻ 0.05 and r ϭ Ϫ0.50, p Ͻ 0.05) both before and after adjustments for energy balance. Baseline plasma leptin concentration, adjusted for differences in FM, was inversely related to the size of weight loss after 8 weeks (r ϭ Ϫ0.41, p ϭ 0.07), 16 weeks (r ϭ Ϫ0.51, p Ͻ 0.05), and 24 weeks (r ϭ Ϫ0.50, p Ͻ 0.05). Discussion: The present study suggests that leptin may have a stimulating effect on fat oxidation in obese subjects. A low leptin level for a given FM was associated with a greater weight loss, suggesting that obese subjects with greater leptin sensitivities are more successful in reducing weight.

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“…The most likely reason for this was the lower pulse-to-noise ratio present at low leptin secretion rates (19). Sinha et al (27) have recently reported a nocturnal rise in serum leptin in lean and obese nondiabetic subjects, and in obese diabetic patients who ate three meals and one snack. These authors were unable to establish circadian rhythmicity because of the shortness of blood sampling.…”

Section: Discussionmentioning

confidence: 99%

Effects of prolonged hyperinsulinemia on serum leptin in normal human subjects.

Boden¹,

Chen²,

Kolaczynski³

et al. 1997

J. Clin. Invest.

261

134

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We have studied the effect of prolonged hyperinsulinemia and hyperglycemia on serum leptin levels in young nonobese males during 72-h euglycemic-hyperinsulinemic and hyperglycemic ( ‫ف‬ 8.5 and 12.6 mM) clamps. Hyperinsulinemia increased serum leptin concentrations (by RIA) dosedependently. An increase in serum insulin concentration of Ͼ 200 pM for Ͼ 24 h was needed to significantly increase serum leptin. An increase of ‫ف‬ 800 pM increased serum leptin by ‫ف‬ 70% over 72 h. Changes in plasma glucose concentrations (from ‫ف‬ 5.0 to ‫ف‬ 12.6 mM) or changes in plasma FFA concentrations (from Ͻ 100 to Ͼ 1,000 M) had no effect on serum leptin. Serum leptin concentrations changed with circadian rhythmicity. The cycle length was ‫ف‬ 24 h, and the cycle amplitude (peak to trough) was ‫ف‬ 50%. The circadian leptin cycles and the circadian cycles of total body insulin sensitivity (i.e., GIR, the glucose infusion rates needed to maintain euglycemia during hyperinsulinemic clamping) changed in a mirror image fashion. Moreover, GIR decreased between Days 2 and 3 (from 11.4 Ϯ 0.2 to 9.8 Ϯ 0.2 mg/kg min, P Ͻ 0.05) when mean 24-h leptin levels reached a peak. In summary, we found ( a ) that 72 h of hyperinsulinemia increased serum leptin levels dose-dependently; ( b ) that hyperglycemia or high plasma FFA levels did not affect leptin release; ( c ) that leptin was released with circadian rhythmicity, and ( d ) that 24-h leptin cycles correlated inversely with 24-h cycles of insulin sensitivity. We speculate that the close positive correlation between body fat and leptin is mediated, at least in part, by insulin. ( J. Clin. Invest. 1997. 100:1107-1113.) Key words: hyperglycemia • free fatty acids • circadian leptin release • insulin resistance

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Nocturnal rise of leptin in lean, obese, and non-insulin-dependent diabetes mellitus subjects.

Cited by 721 publications

References 27 publications

Adiponectin complexes in human cerebrospinal fluid: distinct complex distribution from serum

Adiponectin complexes in human cerebrospinal fluid: distinct complex distribution from serum

Leptin Levels Are Associated with Fat Oxidation and Dietary‐Induced Weight Loss in Obesity

Effects of prolonged hyperinsulinemia on serum leptin in normal human subjects.

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