Adipose tissue leptin production and plasma leptin kinetics in humans

Klein, Samuel; Coppack, Simon W.; Mohamed‐Ali, Vidya; Landt, Michael

doi:10.2337/diabetes.45.7.984

Cited by 298 publications

(157 citation statements)

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“…We measured plasma leptin concentrations in a search for the putative signal which decreased HSL activity during Intralipid infusion, in view of increasing evidenced that leptin production is regulated by nutrient availability, 38 that certain variants of the leptin receptor are expressed on adipocytes 39 and that leptin itself is a stimulator of lipolysis. 8,9 Our results con®rm consistent leptin release by human adipose tissue in vivo, only observed previously in the fasting state 40 or after carbohydrate ingestion. 41 Although there was no signi®cant change in leptin secretion during Intralipid infusion, in keeping with the suggestion that nutrient availability or insulin exert relatively slow effects on leptin expression, 42 the numbers studied are small and these results should be treated only as preliminary.…”

Section: Discussionsupporting

confidence: 71%

Peripheral fat metabolism during infusion of an exogeneous triacylglycerol emulsion

Samra¹,

Giles²,

Summers³

et al. 1998

Int J Obes

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OBJECTIVE: To test the hypothesis that intravenous infusion of lipid would bring about changes in adipose tissue metabolism, which would tend to spare net fat mobilization, and to attempt to identify the mediators of such responses. DESIGN: The triacylglycerol (TG) emulsion, Intralipid, was infused and metablic changes in subcutaneous adipose tissue and forearm muscle were assessed by measurements of arterio-venous differences. SUBJECTS: Six normal male subjects aged 21 ± 37 y, with body mass index (BMI) 23.0 ± 25.9 kgam 2 . RESULTS: Plasma TG and non-esteri®ed fatty acid (NEFA) concentrations rose during infusion as expected. The rise in systemic plasma NEFA concentration occurred despite decreased NEFA release from adipose tissue. Intralipid infusion resulted in a suppression of intracellular lipolysis in adipose tissue, by mechanisms which are not clear. Plasma leptin concentrations, measured in a search for the regulator of lipolysis, showed consistent leptin release from adipose tissue which did not change signi®cantly with time. CONCLUSION: The suppression of intracellular lipolysis in adipose tissue during Intralipid infusion is a new observation and may re¯ect a novel mechanism for regulation of fat storage.

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Section: Discussionsupporting

confidence: 71%

Peripheral fat metabolism during infusion of an exogeneous triacylglycerol emulsion

Samra¹,

Giles²,

Summers³

et al. 1998

Int J Obes

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“…The obese gene product, leptin, is secreted and exclusively expressed by AT [2, 9-13]. Numerous studies have now reported strong positive correlations between total adiposity and fasting plasma leptin concentrations or its AT mRNA levels [14][15][16][17][18][19][20][21]. In the present study, an increased body FM was associated with higher plasma leptin concentrations in men and women.…”

Section: Discussionsupporting

confidence: 64%

“…Leptin is secreted by white adipose cells and is exclusively expressed in adipose tissue (AT) [2,[9][10][11][12][13]. In this regard, numerous studies have reported a strong relationship between adiposity and plasma leptin concentrations or its AT mRNA levels [14][15][16][17][18][19][20][21]. Furthermore, expression of the obese gene is Diabetologia (1997Diabetologia ( ) 40: 1178Diabetologia ( -1184 Plasma leptin concentrations: gender differences and associations with metabolic risk factors for cardiovascular disease Summary The cloning of the obese gene and the characterization of its protein product, leptin, has permitted the study of a new hormone potentially involved in the regulation of adipose tissue mass.…”

mentioning

confidence: 99%

Plasma leptin concentrations: gender differences and associations with metabolic risk factors for cardiovascular disease

et al. 1997

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Obesity results from an imbalance between energy intake and expenditure. Furthermore, obesity has long been recognized to have detrimental effects on health including an increased risk of cardiovascular disease (CVD) [1]. In this regard, the recent cloning of the mouse (ob) and human (OB) obese genes and the characterization of its protein product, leptin [2], has been a breakthrough of potentially great importance for the understanding of the pathophysiology of obesity.Leptin has been shown to lower body weight by reducing food intake and increasing energy expenditure in leptin-deficient obese mice (ob/ob) and also to normalize blood glucose levels in the same animals [2][3][4][5][6][7][8]. Leptin is secreted by white adipose cells and is exclusively expressed in adipose tissue (AT) [2,[9][10][11][12][13]. In this regard, numerous studies have reported a strong relationship between adiposity and plasma leptin concentrations or its AT mRNA levels [14][15][16][17][18][19][20][21]. Furthermore, expression of the obese gene is Diabetologia (1997Diabetologia ( ) 40: 1178Diabetologia ( -1184 Plasma leptin concentrations: gender differences and associations with metabolic risk factors for cardiovascular disease Summary The cloning of the obese gene and the characterization of its protein product, leptin, has permitted the study of a new hormone potentially involved in the regulation of adipose tissue mass. The present study examined the gender differences in fasting plasma leptin concentration and its relationship to body fatness, adipose tissue distribution and the metabolic profile in samples of 91 men (mean age ± SD: 37.3 ± 4.8 years) and 48 women (38.5 ± 6.8 years). Plasma leptin concentrations were strongly associated with body fat mass measured by underwater weighing [men: r = 0.80, p < 0.0001; women: r = 0.85, p < 0.0001]. In both genders, plasma leptin levels were also strongly correlated with waist girth as well as cross-sectional areas of abdominal subcutaneous and visceral adipose tissue measured by computed tomography. Women had, on average, plasma leptin concentrations that were three times higher than men. Furthermore, this gender difference remained significant when comparing men and women matched for similar levels of body fat mass. The associations between plasma leptin and lipoprotein concentrations were dependent of adiposity. In both men and women, elevated fasting plasma leptin levels were associated with higher plasma insulin concentrations, but only in women was the association maintained after correction for fat mass. Thus, results of the present study show that women have higher plasma leptin levels compared to men, independent of the concomitant variation in total body fat mass. Furthermore, our results also suggest that, in women, the association between plasma leptin and insulin concentrations is independent of adiposity, a finding which provides further support to the observation that adipose tissue leptin secretion may be upregulated by insulin.

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“…Second, during comparable hyperinsulinemia, serum leptin levels rose equally regardless of whether glucose concentrations were high or basal; and lastly, the increase in serum leptin during combined hyperinsulinemia/hyperglycemia (protocol 5) was the same as the increase during euglycemic hyperinsulinemia (protocol 2). Assuming that insulin did not affect leptin clearance, for which there is some evidence (20), the data indicated that prolonged hyperinsulinemia stimulated leptin secretion independent of hyperglycemia.…”

Section: Discussionmentioning

confidence: 93%

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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Adipose tissue leptin production and plasma leptin kinetics in humans

Cited by 298 publications

References 0 publications

Peripheral fat metabolism during infusion of an exogeneous triacylglycerol emulsion

Peripheral fat metabolism during infusion of an exogeneous triacylglycerol emulsion

Plasma leptin concentrations: gender differences and associations with metabolic risk factors for cardiovascular disease

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

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