Acute and chronic effects of insulin on leptin production in humans: Studies in vivo and in vitro

Kolaczynski, Jerzy W.; Nyce, M. R.; Considine, Robert V.; Boden, G.; Nolan, J. J.; Henry, R.; Mudaliar, S. R.; Olefsky, J.; F., J.

doi:10.2337/diabetes.45.5.699

Cited by 278 publications

(252 citation statements)

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“…Together, these findings suggested that relatively large increases in serum insulin levels (Ͼ 200 pM) were needed for relatively long periods of time (Ͼ 24 h) before serum leptin levels rose significantly. These results are in accord with reports by several groups, who, with one exception, all failed to find effects of acute (up to 5 h) hyperinsulinemia on leptin levels (10)(11)(12)(13)(14)(15)(16). The sole exception, a study by Utriainen et al (16), reported an ‫ف‬ 50% increase in serum leptin after 4 h of unphysiologic high insulin levels ‫ف(‬ 2,800 pM).…”

Section: Discussionsupporting

confidence: 89%

“…Possible causes for the precipitous decrease in leptin during fasting include changes in serum insulin and/or glucose concentrations. Insulin, because of its close relationship to appetite and body weight control (9), has been scrutinized by several groups (10)(11)(12)(13)(14)(15)(16). All but one (16) found no acute (up to 5 h) effects of hyperinsulinemia on serum leptin concentrations.…”

Section: Introductionmentioning

confidence: 99%

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

Boden¹,

Chen²,

Kolaczynski³

et al. 1997

J. Clin. Invest.

264

140

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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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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

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

Boden¹,

Chen²,

Kolaczynski³

et al. 1997

J. Clin. Invest.

264

140

View full text Add to dashboard Cite

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“…Third, the levels of adiponectin were very low in the preovulatory follicular fluid consistent with absent or undetectable expression of this protein in human granulosa cells [20]. Lastly, it is well established that insulin can stimulate leptin production both in vivo and in vitro [13], whereas adiponectin may potentiate insulin sensitivity at the tissue level but not necessarily affect its expression [2,22]. This is consistent with our observation that FF leptin and the L:A ratio positively correlated with FF insulin, while adiponectin and insulin were indirectly associated.…”

Section: Discussionmentioning

confidence: 67%

Ovarian adipocytokines are associated with early in vitro human embryo development independent of the action of ovarian insulin

Ferin

Sauer

et al. 2012

J Assist Reprod Genet

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Purpose We aimed to characterize the association between levels of serum and follicular fluid (FF) adipocytokines, reflected by the leptin to adiponectin ratio (L:A ratio), and oocyte quality and in vitro embryo development in women undergoing assisted reproduction. We also aimed to assess whether follicular hormonal pathways mediate this interaction. Methods We prospectively collected FF from up to four individual preovulatory follicles (n076) and fasting sera from women (n031) without endocrinopathies undergoing in vitro fertilization (IVF) at a university-based center for assisted reproduction. Leptin, total adiponectin, insulin, insulin-like growth factor 1 (IGF-1), and ovarian steriods were measured using enzyme immunoassay. Oocyte maturity, fertilization, and embryo development were assessed. Results FF leptin was similar to serum levels while FF adiponectin was lower. FF leptin (27.10±4.05 ng/mL) and the L:A ratio (11.48E−3±2.57E−3) were related to FF insulin (R 2 00.370 and 0.419, p<0.001) but not to ovarian steroids or IGF-1, whereas FF adiponectin ( 4.22±0.52 ug/mL) correlated only with leptin (R 2 0−0.138, p00.001). Oocytes from a high FF L:A ratio environment were 81 % (RR 1.81 [95%CI 0.97-3.37]) more likely to undergo successful cleavage and 117 % (RR 2.17 [95 % CI 1.06-4.44]) more likely to obtain viable cleavage morphology compared to a low FF L:A ratio environment, even when adjusted for FF insulin, an independent predictor of cleavage. Conclusions Certain adipocytokines, particularly the L:A ratio in the FF of the preovulatory follicle, are related to successful in vitro embryo development. This action may be independent of FF insulin.

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“…Noteworthy in the present study is the finding that only serum T3 levels were independently correlated with plasma leptin levels (r ¼ 0.928, P < 0.0001) in multiple regression analyses after adjustment of the time course and BMI, raising the possibility that T3 levels during LCD may play a crucial role in regulating plasma leptin levels. However, this does not exclude the possibility that insulin and NEFA may affect plasma leptin levels (Kolaczynski et al, 1996c;Rentsch & Chiesi, 1996).…”

Section: Clinical Implications Of Leptinmentioning

confidence: 93%

“…Several studies have demonstrated that the leptin gene expression is positively regulated by insulin both in vivo (Saladin et al, 1995;Kolaczynski et al, 1996c) and in vitro (Kolaczynski et al, 1996c;Leroy et al, 1996). Plasma leptin levels decrease after fasting and increase by refeeding in humans (Kolaczynski et al, 1996a,b;Boden et al, 1996;Dubuc et al, 1998;Geldszus et al, 1996;Wadden et al, 1998) and rodents (Frederich et al, 1995), which parallels the change in plasma insulin levels (Kolaczynski et al, 1996b).…”

Section: Clinical Implications Of Leptinmentioning

confidence: 97%

Clinical implications of leptin and its potential humoral regulators in long-term low-calorie diet therapy for obese humans

et al. 2002

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Objective: To address the clinical implications of leptin and to re-examine the relationship between leptin and its potential humoral regulators such as insulin, nonesterified fatty acids (NEFA) and triiodothyronine (T3) in low-calorie diet (LCD) for obese humans. Design: Longitudinal study. Setting: University and foundation hospitals. Subjects: Ten obese men and 10 premenopausal obese women. Interventions: Five men and five women took 800 kcal=day LCD and another five men and five women took 1400 kcal=day balanced deficit diet (BDD) during 4 weeks. Results: Plasma leptin levels in the LCD group decreased more markedly (46.2 AE 14.6 to 13.2 AE 3.6 ng=ml) than that expected for the decrement in percentage fat (39.0 AE 1.7 to 35.9 AE 1.7%) and body mass index (BMI; 35.4 AE 2.4 to 33.1 AE 2.2 kg=m 2 ), while that in the BDD group did not decrease significantly (14.9 AE 3.5 to 13.4 AE 2.8 ng=ml). The ratio of the decrease in leptin levels to that of BMI during the first week was significantly greater than that during the following 3 weeks (39.5 AE 2.7 vs 29.3 AE 2.1%, P ¼ 0.017). The plasma insulin and T3 levels also fell substantially in the first week and continued to decrease during the entire course. Plasma leptin levels measured weekly in each subject were correlated well with insulin (r ¼ 0.586, P ¼ 0.0003) and T3 (r ¼ 0.785, P ¼ 0.0004). Multiple regression analyses after adjustment for the time course and BMI revealed that serum levels of T3 were independently correlated with plasma leptin levels (r ¼ 0.928, P < 0.0001). The plasma NEFA level was markedly elevated during the first 2 weeks and decreased thereafter. Conclusions: A rapid fall in leptin during the first week of LCD, coordinated by insulin, T3 and NEFA, should be beneficial for responding to decreased energy intake. Inversely, in view of the powerful effect of leptin on energy dissipation, the present findings suggest the potential usefulness of leptin in combination with caloric restriction for the treatment of obesity.

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Acute and chronic effects of insulin on leptin production in humans: Studies in vivo and in vitro

Cited by 278 publications

References 0 publications

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

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

Ovarian adipocytokines are associated with early in vitro human embryo development independent of the action of ovarian insulin

Clinical implications of leptin and its potential humoral regulators in long-term low-calorie diet therapy for obese humans

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