Search Results
Search for other papers by K Alexander H Iwen in
Google Scholar
PubMed
Search for other papers by Oezge Senyaman in
Google Scholar
PubMed
Search for other papers by Arne Schwartz in
Google Scholar
PubMed
Search for other papers by Maren Drenckhan in
Google Scholar
PubMed
Search for other papers by Britta Meier in
Google Scholar
PubMed
Search for other papers by Dirk Hadaschik in
Google Scholar
PubMed
Search for other papers by Johannes Klein in
Google Scholar
PubMed
maximal increase in 1450% after 4 h ( Fig. 4 E). ACTH stimulation increases UCP-1 mRNA in brown adipocytes The thermogenic brown adipose tissue contributes to energy balance in small mammals and may be associated with insulin sensitivity in human adults
Search for other papers by Riccardo Dore in
Google Scholar
PubMed
Search for other papers by Luka Levata in
Google Scholar
PubMed
Search for other papers by Sogol Gachkar in
Google Scholar
PubMed
Search for other papers by Olaf Jöhren in
Google Scholar
PubMed
Search for other papers by Jens Mittag in
Google Scholar
PubMed
Search for other papers by Hendrik Lehnert in
Google Scholar
PubMed
Search for other papers by Carla Schulz in
Google Scholar
PubMed
regulation of energy homeostasis. However, the underlying mechanisms are poorly understood. In the brain, and in agreement with its role in the control of energy balance, NUCB2/nesfatin-1 is highly expressed in several hypothalamic nuclei such as
Frontier Science Research Center, Department of Food Science and Human Nutrition, Faculty of Food Science and Nutrition, University of Miyazaki, Miyazaki 889-1692, Japan
Search for other papers by Cho-Rong Bae in
Google Scholar
PubMed
Search for other papers by Kazuya Hasegawa in
Google Scholar
PubMed
Search for other papers by Sayaka Akieda-Asai in
Google Scholar
PubMed
Search for other papers by Yurie Kawasaki in
Google Scholar
PubMed
Frontier Science Research Center, Department of Food Science and Human Nutrition, Faculty of Food Science and Nutrition, University of Miyazaki, Miyazaki 889-1692, Japan
Search for other papers by Kazuyo Senba in
Google Scholar
PubMed
Search for other papers by Youn-Soo Cha in
Google Scholar
PubMed
Search for other papers by Yukari Date in
Google Scholar
PubMed
. Although the energy balance of SP rats did not differ from that of CP rats, SP rats showed insulin resistance and increased levels of factors involved in lipogenesis. Our results indicate that the texture of absorbable food such as SP contributes to the
Search for other papers by Nava Chapnik in
Google Scholar
PubMed
Search for other papers by Yoni Genzer in
Google Scholar
PubMed
Robert H. Smith Faculty of Agriculture, Fritz Haber Center for Molecular Dynamics, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot 76100, Israel
Search for other papers by Avraham Ben-Shimon in
Google Scholar
PubMed
Robert H. Smith Faculty of Agriculture, Fritz Haber Center for Molecular Dynamics, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot 76100, Israel
Search for other papers by Masha Y Niv in
Google Scholar
PubMed
Search for other papers by Oren Froy in
Google Scholar
PubMed
, and possibly safer, alternative for type II diabetes and obesity drug development ( Hardie 2007 ). AMPK is a regulator of energy balance at both the cellular and the whole-body levels ( Carling et al . 2011 , Hardie 2011 ). Typically quiescent under
Search for other papers by C Nilsson in
Google Scholar
PubMed
Search for other papers by D Swolin-Eide in
Google Scholar
PubMed
Search for other papers by C Ohlsson in
Google Scholar
PubMed
Search for other papers by E Eriksson in
Google Scholar
PubMed
Search for other papers by HP Ho in
Google Scholar
PubMed
Search for other papers by P Bjorntorp in
Google Scholar
PubMed
Search for other papers by A Holmang in
Google Scholar
PubMed
Leptin is involved in regulating food intake, energy balance and bone formation. Increasing evidence suggests that leptin is also involved in fetal growth and development. The aim of this study was to determine if increased maternal leptin is followed by changes in body composition, skeletal growth or hormonal regulation in the adult rat offspring. Pregnant rats were given injections of either human recombinant leptin (3.5 mg/kg, i.p.) or vehicle on days 8, 10 and 12 of gestation. Both genders of leptin-exposed offspring showed significantly reduced adipose tIssue weight at adult age. Skeletal growth and cortical bone dimensions were significantly reduced. Circulating testosterone levels were significantly increased in female leptin-exposed offspring, and male leptin-exposed offspring had significant testicular enlargement. No significant effects were seen on circulating leptin levels or hypothalamic protein levels of the leptin receptor. The results demonstrate that maternally administered leptin is involved in fetal growth and development, leading to lean offspring with reduced skeletal growth.
Search for other papers by RG Denis in
Google Scholar
PubMed
Search for other papers by G Williams in
Google Scholar
PubMed
Search for other papers by RG Vernon in
Google Scholar
PubMed
The factors regulating serum leptin concentration and its relationship to the hyperphagia of lactation have been investigated in rats. Lactation results in hypoleptinaemia and loss, or at least marked attenuation, of the nocturnal rise in serum leptin. Litter removal resulted in a fall in food intake and restoration of the nocturnal rise in serum leptin. Returning the litter to the mother after a 48-h absence increased food intake and began to reinitiate milk production, but the nocturnal serum leptin levels were still increased at 48 h after litter restoration. Adjusting litter size to four, eight, ten or fourteen pups at parturition resulted in different rates of litter growth and food intake during the subsequent lactation, but had no effect on the degree of hypoleptinaemia. Reducing litter size from ten to four pups at mid-lactation resulted in a transient increase in both serum leptin and pup growth rate, while food intake fell to a level found in rats suckling four pups throughout lactation. Reducing milk production by injection of bromocriptine increased serum leptin, but did not restore the nocturnal rise in serum leptin; food intake decreased, but remained much higher than in non-lactating rats. Feeding a varied, high-energy diet resulted in a decrease in the weight of food ingested, but no change in calorie intake, and had no effect on the hypoleptinaemia. These studies suggested that the hypoleptinaemia of lactating rats is due to negative energy balance, but the loss of the nocturnal rise in serum leptin is due to the suckling stimulus. The negative energy balance of lactation does not appear to be caused by a physical constraint on food intake. While the hypoleptinaemia should facilitate the hyperphagia of lactation, other orexigenic signals must also be involved.
Institute for Health and Sport (iHeS), Victoria University, Melbourne, Victoria, Australia
Search for other papers by Amanda J Genders in
Google Scholar
PubMed
Search for other papers by Timothy Connor in
Google Scholar
PubMed
Search for other papers by Shona Morrison in
Google Scholar
PubMed
Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia
Search for other papers by Simon T Bond in
Google Scholar
PubMed
Search for other papers by Brian G Drew in
Google Scholar
PubMed
Search for other papers by Peter J Meikle in
Google Scholar
PubMed
Search for other papers by Kirsten F Howlett in
Google Scholar
PubMed
Search for other papers by Sean L McGee in
Google Scholar
PubMed
Protein kinase D (PKD) is emerging as an important kinase regulating energy balance and glucose metabolism; however, whether hepatic PKD activity can be targeted to regulate these processes is currently unclear. In this study, hepatic PKD activity was reduced using adeno-associated virus vectors to express a dominant-negative (DN) version of PKD1, which impairs the action of all three PKD isoforms. In chow-fed mice, hepatic DN PKD expression increased whole-body glucose oxidation, but had only mild effects on glucose and insulin tolerance and no effects on glucose homeostasis following fasting and refeeding. However, circulating VLDL cholesterol was reduced under these conditions and was associated with hepatic fatty acid accumulation, but not lipids involved in lipoprotein synthesis. The limited effects on glucose homeostasis in DN PKD mice was despite reduced expression of gluconeogenic genes under both fasted and refed conditions, and enhanced pyruvate tolerance. The requirement for PKD for gluconeogenic capacity was supported by in vitro studies in cultured FAO hepatoma cells expressing DN PKD, which produced less glucose under basal conditions. Although these pathways are increased in obesity, the expression of DN PKD in the liver of mice fed a high-fat diet had no impact on glucose tolerance, insulin action, pyruvate tolerance or plasma VLDL. Together, these data suggest that PKD signalling in the liver regulates metabolic pathways involved in substrate redistribution under conditions of normal nutrient availability, but not under conditions of overnutrition such as in obesity.
Search for other papers by ELIZABETH HERVEY in
Google Scholar
PubMed
Search for other papers by G. R. HERVEY in
Google Scholar
PubMed
SUMMARY
The effects of progesterone administration on the weight and composition of the body have been studied in rats. Female rats injected with 5 mg. progesterone/day initially gained weight at an average rate of 2 g./day, compared with 0·4 g./day for controls. When treatment was continued for a month or more their weight stabilized at 40–50 g. above the control level. The bodies of the progesterone-treated rats contained increased amounts of water, fat and solids other than fat. These effects were smoothly related to the dose of progesterone.
In terms of percentage composition, fat increased at the expense of the other two constituents. The composition of the fat-free solids did not change, but the proportion of water in the fat-free body increased. About a tenth of the gain of live weight was accounted for by an increase in the contents of the alimentary tract. The composition of the rest was equivalent, typically, to 43% lean tissue, 26% water additional to that in the lean tissue, and 31% fat.
Male rats treated with progesterone showed no changes other than a small gain of water.
It seems likely that in females progesterone reproduces the changes in body composition which occur in pregnancy. The gain of lean tissue seems to reflect increased growth it, and the accumulation of fat, may both be consequences of the production of a positive energy balance.
Search for other papers by Martina Holubová in
Google Scholar
PubMed
Department of Analytical Chemistry, University of Chemistry and Technology, Prague, Czech Republic
Search for other papers by Jana Zemenová in
Google Scholar
PubMed
Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
Search for other papers by Barbora Mikulášková in
Google Scholar
PubMed
Search for other papers by Vladimíra Panajotova in
Google Scholar
PubMed
Search for other papers by Jiří Stöhr in
Google Scholar
PubMed
Search for other papers by Martin Haluzík in
Google Scholar
PubMed
Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
Search for other papers by Jaroslav Kuneš in
Google Scholar
PubMed
Search for other papers by Blanka Železná in
Google Scholar
PubMed
Search for other papers by Lenka Maletínská in
Google Scholar
PubMed
Anorexigenic neuropeptides produced and acting in the brain have the potential to decrease food intake and ameliorate obesity, but are ineffective after peripheral application, owing to a limited ability to cross the blood–brain barrier. We have designed lipidized analogs of prolactin-releasing peptide (PrRP), which is involved in energy balance regulation as demonstrated by obesity phenotypes of both Prrp-knockout and Prrp receptor-knockout mice. The aim of this study was to characterize the subchronic effect of a palmitoylated PrRP analog in two rat models of obesity and diabetes: diet-induced obese Sprague–Dawley rats and leptin receptor-deficient Zucker diabetic (ZDF) rats. In the rats with diet-induced obesity (DIO), a two-week intraperitoneal treatment with palmitoylated PrRP lowered food intake by 24% and body weight by 8%. This treatment also improved glucose tolerance and tended to decrease leptin levels and adipose tissue masses in a dose-dependent manner. In contrast, in ZDF rats, the same treatment with palmitoylated PrRP lowered food intake but did not significantly affect body weight or glucose tolerance, probably in consequence of severe leptin resistance due to a nonfunctional leptin receptor. Our data indicate a good efficacy of lipidized PrRP in DIO rats. Thus, the strong anorexigenic, body weight-reducing, and glucose tolerance-improving effects make palmitoylated PrRP an attractive candidate for anti-obesity treatment.
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Uxía Gurriarán-Rodríguez in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Omar Al-Massadi in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Ana Belén Crujeiras in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Carlos S Mosteiro in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by María Amil-Diz in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Daniel Beiroa in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Rubén Nogueiras in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Luisa María Seoane in
Google Scholar
PubMed
Search for other papers by Rosalía Gallego in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Yolanda Pazos in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Felipe F Casanueva in
Google Scholar
PubMed
Área de Endocrinología Molecular y Celular, CIBER Fisiopatología de la Obesidad y Nutrición, Departamento de Fisiología, Departamento de Ciencias Morfológicas, Departamento de Medicina, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago, Servicio Gallego de Salud (SERGAS), Santiago de Compostela, Spain
Search for other papers by Jesús P Camiña in
Google Scholar
PubMed
This study aimed to investigate the role of preproghrelin-derived peptides in adipogenesis. Immunocytochemical analysis of 3T3-L1 adipocyte cells showed stronger preproghrelin expression compared with that observed in 3T3-L1 preadipocyte cells. Insulin promoted this expression throughout adipogenesis identifying mTORC1 as a critical downstream substrate for this profile. The role of preproghrelin-derived peptides on the differentiation process was supported by preproghrelin knockdown experiments, which revealed its contribution to adipogenesis. Neutralization of endogenous O-acyl ghrelin (acylated ghrelin), unacylated ghrelin, and obestatin by specific antibodies supported their adipogenic potential. Furthermore, a parallel increase in the expression of ghrelin-associated enzymatic machinery, prohormone convertase 1/3 (PC1/3) and membrane-bound O-acyltransferase 4 (MBOAT4), was dependent on the expression of preproghrelin in the course of insulin-induced adipogenesis. The coexpression of preproghrelin system and their receptors, GHSR1a and GPR39, during adipogenesis supports an autocrine/paracrine role for these peptides. Preproghrelin, PC1/3, and MBOAT4 exhibited dissimilar expression depending on the white fat depot, revealing their regulation in a positive energy balance situation in mice. The results underscore a key role for preproghrelin-derived peptides on adipogenesis through an autocrine/paracrine mechanism.
