The Effects of Insulin, Glucose, and Pyruvate on the Kinetics of Leptin Secretion

Levy, James R.; Stevens, Wayne

doi:10.1210/endo.142.8.8313

Cited by 45 publications

(34 citation statements)

References 24 publications

(32 reference statements)

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“…The brain could monitor adipocyte function via sensory innervation of adipose tissue (34). Adipose tissue can also communicate with the brain through changes in circulating leptin levels because adipocyte leptin production responds to changes in substrate oxidation (35)(36)(37).…”

Section: Discussionmentioning

confidence: 99%

Effect of Food Restriction and Intense Physical Training on Estrous Cyclicity and Plasma Leptin Concentrations in Rats

Santos

Silva

Bacurau

et al. 2011

J Nutr Sci Vitaminol

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SummaryIntense physical training and dietary energy restriction have been associated with consequences such as nutritional amenorrhea. We investigated the effects of intense physical training, food restriction or the combination of both strategies on estrous cyclicity in female rats, and the relationship between leptin ad these effects. Twenty-seven female Wistar rats were distributed into four groups: SF: sedentary, fed ad libitum; SR: sedentary subjected to 50% food restriction (based on the food intake of their fed counterparts); TF: trained (physical training on a motor treadmill with a gradual increase in speed and time), fed ad libitum; TR: trained with 50% food restriction. We analysed estrous cyclicity, plasma leptin and estradiol as well as chemical composition of the carcass, body weight variation, and weight of ovaries and perirenal adipose tissue. Data demonstrate that physical training alone was not responsible for significant modifications in either carcass chemical composition or reproductive function. Food restriction reduced leptin levels in all animals and interrupted the estrous cyclicity in some animals, but only the combination of food restriction and physical training was capable of interrupting the estrous cyclicity in all animals. Leptin was not directly related to estrous cyclicity. From our findings, it may be concluded that there is an additive or synergistic effect of energy intake restriction and energy expenditure by intense physical training on estrous cyclicity. Leptin appears to be one among others factors related to estrous cycle, but it probably acts indirectly. Key Words energy intake, body composition, estrous cycle, leptin, physical exercise Some female athletes are constantly under pressure to achieve and/or to maintain low body weight, leading to potentially harmful patterns of restricted dieting and over exercising. Some of the health consequences of long-term energy restriction include poor nutritional status and risk of exercise-induced amenorrhea ( 1 , 2 ). In humans, this condition is characterized by the absence of menstruation for 90 d or more.Based on epidemiological data, Frisch ( 3 ) reported that, in women and girls, body fat content and ovulatory cyclicity were positively associated. However, one or more main signals that centrally indicates the availability of energy is still unknown ( 4 ). Since physical activity may reduce leptin mRNA expression ( 5 , 6 ) and athletes that train intensively, under restricted calorie intake, present a higher percentage of amenorrhea than sedentary women ( 7 ), it may be speculated that leptin is involved in the transduction of the energy availability signals.Studies on the effects of exercise, reproductive function and leptin response have been hindered by the inability to disassociate the effects of exercise itself from other confusing factors. These factors could be related to energy intake below the requirements or different hormones involved ( 8 , 9 ). It is not clear whether the reproductive functions are interrupted due...

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Section: Discussionmentioning

confidence: 99%

Effect of Food Restriction and Intense Physical Training on Estrous Cyclicity and Plasma Leptin Concentrations in Rats

Santos

Silva

Bacurau

et al. 2011

J Nutr Sci Vitaminol

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“…Furthermore, it has been suggested that the insulin effect on leptin depends on insulin-stimulated glucose uptake and metabolism in rat adipocytes (42,55). Mueller et al (55) concluded that insulin's effect on glucose metabolism explains its ability to stimulate leptin gene expression via a SP-1 site and thus its increased release.…”

Section: Nutrients May Signal Alterations In Leptin Productionmentioning

confidence: 99%

“…Leptin exists in different compartments from other adipocyte secretory products, namely lipoprotein lipase, adiponectin, or glucose transporter 4 (3,6,67). Inhibition of vesicular trafficking with Brefeldin A (49) or monensin (42) blocks leptin release into medium and leads to its intracellular accumulation, indicating that leptin secretion is regulated by the classical secretory pathway. However, leptin does not appear to colocalize within Golgi (3), and Roh et al (67) suggested that, at least in adipocytes from young rats, separate leptin storage vesicles may exist.…”

Section: Regulation Of Leptin Release At Posttranslational Stepsmentioning

confidence: 99%

Integration of hormonal and nutrient signals that regulate leptin synthesis and secretion

Lee¹,

Fried²

2009

American Journal of Physiology-Endocrinology and Metabolism

112

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Lee M-J, Fried SK. Integration of hormonal and nutrient signals that regulate leptin synthesis and secretion. Am J Physiol Endocrinol Metab 296: E1230 -E1238, 2009. First published March 24, 2009 doi:10.1152/ajpendo.90927.2008.-This review summarizes recent advances in our understanding of the pre-and posttranscriptional mechanisms that regulate leptin production and secretion in adipocytes. Basal leptin production is proportional to the status of energy stores, i.e., fat cell size, and this is mainly regulated by alterations in leptin mRNA levels. Leptin mRNA levels are regulated by hormones, including glucocorticoids and catecholamines, but little is known about the transcriptional mechanisms involved. Leptin synthesis and secretion is also acutely modulated in response to hormones such as insulin and the availability of metabolic fuels. Acute variations in leptin production over a time course of minutes to hours are mediated at the levels of both translation and secretion. Increases in amino acids and insulin after a meal activate the mammalian target of rapamycin (mTOR) pathway, leading to an increase in specific rates of leptin biosynthesis. Cross-talk among mTOR, PKA, and AMPactivated protein kinase pathways appears to integrate hormonal and nutrient signals that regulate leptin mRNA translation, at least in part through mechanisms involving its 5Ј-and 3Ј-untranslated regions. In addition, the rate of leptin secretion from preformed stores in response to hormonal cues is also regulated. Insulin stimulates, and adrenergic agonists inhibit, leptin secretion, and this likely contributes to variations in the magnitude of nutrition-related leptin excursions and oscillations. Overall, the study of leptin production has contributed to a deepening understanding of leptin biology and, more broadly, to our understanding of the cellular and molecular mechanisms by which the adipocyte integrates hormonal and nutrient signals to regulate adipokine production. adipose tissue; adrenergic; feeding; insulin; obesity LEPTIN IS A 16-KDA PROTEIN encoded by the obese (lep) gene that is expressed and secreted mainly by adipocytes. When energy stores are low, a fall in leptin decreases thermogenesis, promotes fatty acid (FA) over glucose oxidation, and decreases the activity of the hypothalamic pituitary adrenal and gonadal axes (1). Leptin also modulates the activities of the hematopoietic (5) and immune (52) systems, as well as angiogenesis (7).

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“…For example, Thomas et al (2001) used immunocytochemistry to detect leptin protein at the maternal and fetal interface of the ovine placenta and proposed that leptin may mediate nutrient partitioning to the fetus via interaction with placental leptin receptors. Leptin synthesis is nutritionally sensitive (Levy and Stevens, 2001), with circulating concentrations varying according to the maternal body condition, dietary intake and plasma insulin concentrations (Thomas et al, 2001). Thus, the effects of body condition on leptin function and fetal growth warrant further investigation.…”

Section: Discussionmentioning

confidence: 99%

Effect of maternal body condition on placental and fetal growth and the insulin-like growth factor axis in Dorset ewes

Osgerby¹

2003

Reproduction

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This study investigated the effects of maternal body condition on fetal growth. Fetal and placental parameters from Dorset ewes of body condition score 2.0 (lean, n = 5), 3.5 (moderate, n = 7) and 5.0 (fat, n = 4) at mating were studied on day 65 of gestation. The fetal weight and fetal weight:crown-rump length ratio were greater in fat ewes than in ewes of moderate condition. The raised total and mean placentome weight in fat ewes compared with ewes of moderate condition may have contributed to their increased fetal growth. However, the fetal crown-rump length was not affected. With in situ hybridization, insulinlike growth factor II (IGF-II) mRNA and insulin-like growth factor binding protein 2 (IGFBP-2), -3 and -6 were all detected in the placentome capsule; IGF-II mRNA was also found in the mesoderm of the fetal villi and IGFBP-3 and IGFBP-6 were present in the caruncular stroma of the maternal villi. Ewes of moderate condition, which had the smallest placentae, had the greatest placental expression of IGF-II, IGFBP-2 and IGFBP-3. In the intercotyledonary endometrium, IGFBP-3, IGFBP-5 and uterine milk protein (UTMP) mRNA were all expressed in the glandular epithelium. IGFBP-3 and IGFBP-5 absorbance values were lowest in the lean ewes, whereas UTMP values were highest. Maternal insulin concentrations were greater in fat ewes, whereas plasma glucose and IGF-I concentrations in the fetal compartment were lowest in fat ewes. Therefore, in obese ewes, fetal and placental growth is increased in mid-gestation in association with higher maternal insulin concentrations and lower expression of IGFBPs in the maternal placentomes. Placental and fetal development in lean ewes may be promoted by reduced IGFBP expression in the placentomes and enhanced UTMP production by the endometrial glands. The ewes of moderate condition had the smallest fetuses and placentae coupled with the highest placental expression of IGF-II and IGFBPs.

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The Effects of Insulin, Glucose, and Pyruvate on the Kinetics of Leptin Secretion

Cited by 45 publications

References 24 publications

Effect of Food Restriction and Intense Physical Training on Estrous Cyclicity and Plasma Leptin Concentrations in Rats

Effect of Food Restriction and Intense Physical Training on Estrous Cyclicity and Plasma Leptin Concentrations in Rats

Integration of hormonal and nutrient signals that regulate leptin synthesis and secretion

Effect of maternal body condition on placental and fetal growth and the insulin-like growth factor axis in Dorset ewes

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