Increase in plasma leptin and Lep mRNA concentrations by food intake is dependent on insulin

Patel, Bharati; Koenig, James I.; Kaplan, Lee M.; Hooi, Shing Chuan

doi:10.1016/s0026-0495(98)90247-5

Cited by 50 publications

(31 citation statements)

References 24 publications

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“…Moreover, recent reports indicate that postprandial insulinemia may be an important modulator of the hyperleptinemia induced by dexamethasone (2 1) or feeding (22). Although treatment with exogenous insulin resulted in ambient insulinemia that was higher in the two groups of diabetic patients compared with controls, insulin levels in these patients did not increase further in response to dexamethasone (or meals), and this was associated with failure to augment leptin secretion.…”

Section: Discussionmentioning

confidence: 95%

Basal and Stimulated Plasma Leptin in Diabetic Subjects

Liu¹,

Askari²,

Dagogo‐Jack³

1999

Obesity Research

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LIU, JIANMEI, HASAN ASKARI, AND SAMUEL DAGOGO-JACK. Basal and stimulated plasma leptin in diabetic subjects. Obes Res. 1999;7:537-544. Objective: To determine whether leptin secretion is impaired in diabetes, we compared basal and stimulated plasma leptin levels in diabetic subjects and healthy controls. Research Methods and Procedures: Blood samples for assay of leptin and other hormones were obtained at baseline in 54 diabetic patients and 65 controls, and 8 hours, 16 hours, and 40 hours following ingestion of dexamethasone (4 mg) in 6 healthy and 12 controls. C-peptide status was defined as "negative" if 50.1 ng/mL or "positive" if 20.3 ng/mL, in fasting plasma. Results: Basal plasma leptin levels were 19.7k2.2 ng/mL in nondiabetic subjects, 13.421.5 ng/ml in C-peptide negative (n = 28) and 26.123.7 ng/mL in C-peptide positive (n = 26, p = 0.00 1) diabetic patients. Dexamethasone increased leptin levels of controls (n = 6) to 145217% of baseline values at 8 hours (p=O.O3), 224218% at 16 hours (p=O.Ol), and 134218% at 40 hours ( p = 0.05). The corresponding changes were 108213%, 126+23%, and 98k16% in C-peptide negative (n=6), and 121210%, 144*16% (p=0.03), and 147223% (p=O.11) in C-peptide positive (n=6) diabetic patients, respectively. The peak stimulated leptin levels were lower in the diabetic patients, compared with controls. Plasma insulin increased (p = 0.02) in controls, but not in the diabetic patients, following dexamethasone. Discussion: Although diabetic patients have normal plasma leptin levels under basal conditions, their leptin responses to glucocorticoid are impaired, probably because of the concomitant insulin secretory defect. A subnormal leptin secretory response could worsen obesity and insulin resistance in diabetes.

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Section: Discussionmentioning

confidence: 95%

Basal and Stimulated Plasma Leptin in Diabetic Subjects

Liu¹,

Askari²,

Dagogo‐Jack³

1999

Obesity Research

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“…Insulin has previously been shown to be important in the leptin response to nutritional stimuli, with both sustained hyperinsulinaemia being associated with increased serum leptin levels, and the fall in serum leptin with fasting being attributed to the fall in serum insulin. 2,3,7 Insulin also regulated leptin levels during hyperinsulinaemic clamps in both humans and rodents, with an increased leptin response produced from a greater dose of insulin. 22,23 Glucose has also been postulated as a signal of nutritional status.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] Fasting causes a significant reduction in serum leptin and leptin gene expression. [2][3][4][5][6][7][8] The fasting-induced reduction in leptin gene expression can be reversed by refeeding or the administration of insulin or glucose. 4,5,9 In vitro, leptin secretion is stimulated acutely by both glucose [10][11][12] and insulin [13][14][15][16] and inhibited by nonesterified fatty acids (NEFA).…”

Section: Introductionmentioning

confidence: 99%

Insulin determines leptin responses during a glucose challenge in fed and fasted rats

et al. 2005

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OBJECTIVE: Leptin secretion has been shown to respond acutely to changes in blood glucose and insulin. Nutritional state also has a marked effect on both the level of circulating leptin protein and leptin gene expression. The aim of this study was to assess whether the prior nutritional state altered the leptin secretory response to an acute glucose challenge, and to determine potential mechanisms. DESIGN: Male fed or fasted rats (200-250 g) were administered a single intravenous glucose bolus (1, 4 or 7 g/kg). The serum leptin, glucose, insulin and free fatty acid responses were studied over the following 5 h. The level of leptin gene expression and leptin protein was then determined in the epididymal fat pads, and in fed and fasted untreated rats for basal comparison. RESULTS: Leptin secretion in response to glucose was suppressed in fasted rats following all glucose doses. The total leptin response was correlated with the total insulin response in all conditions (r ¼ 0.85) and with the glucose response in fed rats (r ¼ 0.69). Both leptin gene expression and leptin protein content were lower in basal fasted rats. Leptin gene expression and leptin protein content still remained lower 5 h following a glucose bolus but there was partial reversal of the effects of fasting following the 7 g/kg glucose dose. CONCLUSIONS: Leptin secretion in response to an intravenous glucose bolus was determined by the insulin response and was significantly suppressed in fasted compared to fed rats. In addition to differences in the total insulin response of the animals, lower leptin responses may be facilitated by lower levels of both leptin gene mRNA and pre-existing leptin protein in epididymal adipose tissue of fasted rats.

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“…Rats made insulin de®cient by streptozotocin (STZ) treatment show signi®cantly reduced leptin levels; when these STZ-treated animals receive an insulin injection, leptin secretion increases rapidly again (146,149,150). Similarly, in diabetic rats the reduced plasma leptin levels found under conditions of insulin de®ciency are also raised by insulin treatment (150).…”

Section: Effect Of Insulin On Leptin Secretionmentioning

confidence: 99%

Human leptin: from an adipocyte hormone to an endocrine mediator

2000

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Leptin is a mainly adipocyte-secreted protein that was discovered 5 years ago. Most of the research following this discovery focused on the role of leptin in body weight regulation, aiming to illuminate the pathophysiology of human obesity. However, more and more data are emerging that leptin is not only important in the regulation of food intake and energy balance, but that it also has a function as a metabolic and neuroendocrine hormone. It is now clear that it is especially involved in glucose metabolism, as well as in normal sexual maturation and reproduction. Besides this, interactions with the hypothalamic±pituitary±adrenal, thyroid and GH axes and even with haematopoiesis and the immune system have also been described. It has been shown that leptin secretion by the adipocyte is partly regulated by other hormones, such as insulin, cortisol, and sex steroids, mainly testosterone. Also, other hormones like thyroid hormone and GH are possibly involved in leptin synthesis. Leptin itself exerts effects on different endocrine axes, mainly on the hypothalamic±pituitary±gonadal axis and on insulin metabolism, but also on the hypothalamic±pituitary±adrenal, thyroid and GH axes.Leptin may thus be considered a new endocrine mediator, besides its obvious role in body weight regulation.

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Increase in plasma leptin and Lep mRNA concentrations by food intake is dependent on insulin

Cited by 50 publications

References 24 publications

Basal and Stimulated Plasma Leptin in Diabetic Subjects

Basal and Stimulated Plasma Leptin in Diabetic Subjects

Insulin determines leptin responses during a glucose challenge in fed and fasted rats

Human leptin: from an adipocyte hormone to an endocrine mediator

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