Leptin levels do not change acutely with food administration in normal or obese subjects, but are negatively correlated with pituitary‐adrenal activity

Korbonits, M; Trainer, Peter; Little, John A.; Edwards, R. W. H.; Kopelman, Peter; Besser, G. M.; Švec, František; Grossman, A

doi:10.1046/j.1365-2265.1997.1820979.x

Cited by 129 publications

(98 citation statements)

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“…Table 2 Glucose, insulin and leptin concentration before and after glucose administration (30, 60, 90 and 120 min) in the experimental group of individuals, as well as leptin concentration before and after water administration (controls) 19 In humans, it has also been shown that increasing serum insulin concentrations for a short period of time (5 h) either postprandially or after infusion of insulin does not in¯uence the secretion of leptin. 13,16,18 Our ®nding that there is no signi®cant correlation between leptin and insulin concentrations during glucose loading is in accord with previous data which have shown that insulin does not stimulate endogenous leptin secretion and permits us to postulate that other factors affect both leptin and insulin secretion. Corticosteroids might be one such factor, as well as catecholamines.…”

Section: Discussionsupporting

confidence: 79%

“…They found an increase in insulin concentrations, while leptin concentrations did not change 3 h after food. Korbonits et al 16 provided a mixed meal of 1000 kcal in obese and normal weight individuals and found no changes in leptin concentrations before and after the meal. Also, they did not ®nd any correlation between leptin and glucose, as well as leptin and insulin concentrations.…”

Section: Discussionmentioning

confidence: 99%

“…However, no details were given about the gender and BMI of the individuals investigated. Korbonits et al 16 provided a standard mixed mid-day meal (1000 kcal) in 10 obese females with blood sampled at 20 min intervals from 1 h before lunch (11.00 h) until 3 h post-prandially.…”

Section: Discussionmentioning

confidence: 99%

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Leptin concentrations during oral glucose tolerance test (OGTT) in obese and normal weight women

et al. 1999

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OBJECTIVE: To examine possible changes of leptin concentrations after the acute administration of glucose orally (OGTT). DESIGN: Seventy-®ve grams of glucose were administered per os in one group of obese and normal weight individuals and concentrations of glucose, insulin and leptin were measured at 0, 30, 60, 90 and 120 min. In an age matched control group of individuals with similar BMI water was given and leptin concentrations were measured before and after 30, 60, 90 and 120 min. SUBJECTS: Twenty-seven obese women aged 34 AE 1.57 y with BMI 37.1 AE 0.8 kgam 2 and 16 normal weight women, aged 32 AE 1.13 y with BMI 23.6 AE 0.3 kgam 2 formed the experimental group, while 10 obese and 10 normal weight females with similar age and BMI were used as controls. MEASUREMENTS: Weight, height, BMI, body fat, glucose, insulin and leptin at baseline and during OGTT. Variations of the above parameters were calculated from the area under the curve (AUC). RESULTS: Fasting leptin concentrations and AUC were higher in obese than in normal weight women. In obese women, leptin increased signi®cantly in comparison to its basal concentrations 30 and 60 min after the glucose loading. Insulin was also increased, as expected. No correlation was found between insulin and leptin concentrations after glucose loading. Basal concentrations of leptin did not correlate with those of glucose and insulin. No changes in leptin concentrations were found in normal weight women after OGTT. However, a signi®cant positive correlation was found between insulin and basal leptin. Finally, leptin concentrations did not change in obese and normal weight controls after water administration. CONCLUSION: A signi®cant increase in leptin concentrations was found 30 and 60 min after glucose loading in obese individuals. No such increase was found in normal-weight women.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

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Leptin concentrations during oral glucose tolerance test (OGTT) in obese and normal weight women

et al. 1999

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“…In one patient, 6 months after an insulinoma was surgically removed, insulin concentrations decreased from 16.2 to 7.6 mg/l, leptin decreased about 50 % and the patient's BMI had only decreased from 31 to 28 [45]. In diabetic pregnancies, placenta leptin mRNA and protein increased threefold to fivefold after the women were treated with insulin [46].…”

Section: Regulation Of Leptin By Insulinmentioning

confidence: 99%

Nutritional regulation of leptin in humans

Coleman

Herrmann

1999

Diabetologia

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OverviewPositional cloning of the defective gene in genetically obese ob/ob mice identified leptin as the long-sought hormone that communicates information about adipocyte metabolism to the brain [1]. Supplying leptin to genetically deficient ob/ob mice increases metabolic rate, body temperature and general activity and decreases food intake, body weight and adiposity [1±4]. Additionally, the importance of leptin to reproduction has been highlighted by the lack of sexual maturation in people who are genetically deficient in leptin [5] or the leptin receptor [6]. Although many of leptin's effects are centrally mediated, there is growing evidence that peripheral leptin receptors mediate leptin's proliferative effects on haemopoietic cells [7] and its anti-lipogenic effects on muscle and pancreatic islets [8,9].Because leptin has a critical role in regulating energy metabolism, adipose stores and body weight, questions have been raised concerning the control of leptin synthesis and secretion and the function of leptin in controlling satiety and food intake. Basal or fasting leptin values are higher in women than men, increase during the course of pregnancy and, in both healthy adults and those with Type II (non-insulindependent) diabetes mellitus, are strongly correlated with per cent body fat or BMI [10,11] and adipose tissue mass [12±15]. Despite these strong correlations, people with similar degrees of adiposity have circulating leptin concentrations that vary considerably. Thus, factors other than adipocyte size and fat content must influence leptin production. Further, the regulation of leptin's diurnal pattern of secretion is still to be explained.In this review we summarize current data, primarily from human studies, that address the nutritional controls on leptin synthesis and secretion and point out fruitful areas for future study. Excellent recent reviews should be consulted for information on the leptin receptor, other aspects of leptin's effects, and the relation of leptin to other hormones that regulate food intake and energy expenditure [16±22]. Leptin regulation by fasting, refeeding and overfeedingFasting and refeeding. During short-term energy restriction, plasma leptin concentrations decrease much more than the amount of weight or adipose tissue lost. For example, lean and obese adults who fasted for 52 to 96 h lost less than 4 % of body weight but the leptin concentrations decreased 54 to 72 % [23±25]. In careful long-term studies of lean and obese people who were either losing weight or maintaining a defined weight loss, leptin concentrations were lower during the period of loss than the period of weight maintenance at the same body composition [26]. After a 4 day fast followed by an additional 6 days of fasting during which an intravenous infusion of 5 % glucose was given, leptin increased 80 % within the first 24 h, even though glucose provided only 338 kcal/day [25]. Although it is possible that the previous 4 day fast confounded these results [27], taken together, these studies suggest that ...

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“…Serum leptin levels are raised by insulin treatment, in type 2 as well as type 1 diabetic patients (140,156). One report on a patient with insulinoma reported markedly elevated leptin levels during chronically high insulinaemia, which both dropped after surgical removal (157), also indicating that chronic hyperinsulinaemia increases leptin expression.…”

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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Leptin levels do not change acutely with food administration in normal or obese subjects, but are negatively correlated with pituitary‐adrenal activity

Cited by 129 publications

References 0 publications

Leptin concentrations during oral glucose tolerance test (OGTT) in obese and normal weight women

Leptin concentrations during oral glucose tolerance test (OGTT) in obese and normal weight women

Nutritional regulation of leptin in humans

Human leptin: from an adipocyte hormone to an endocrine mediator

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