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Frontier Science Research Center, Department of Food Science and Human Nutrition, Faculty of Food Science and Nutrition, University of Miyazaki, Miyazaki 889-1692, Japan
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Frontier Science Research Center, Department of Food Science and Human Nutrition, Faculty of Food Science and Nutrition, University of Miyazaki, Miyazaki 889-1692, Japan
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. 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
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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
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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
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, 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
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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.
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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.
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Department of Analytical Chemistry, University of Chemistry and Technology, Prague, Czech Republic
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Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
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Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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.
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Nonalcoholic fatty liver disease (NAFLD) has become a major health problem in developed countries. It has affected more than 30% of the general population and is commonly associated with insulin resistance, which is a major risk factor for the development of type 2 diabetes and a central feature of the metabolic syndrome. Furthermore, accumulating evidences reveal that NAFLD as well as insulin resistance is strongly related to inflammation. Cytokines and adipokines play a pivotal role in inflammatory processes. In addition, these inflammatory mediators regulate various functions including metabolic energy balance, inflammation, and immune response. However, their role in modulating ectopic lipids involved in the development of insulin resistance, such as diacylglycerols and ceramides, remains unknown. The aim of this review is first to describe the pathophysiology of insulin resistance in NAFLD. In particular, we discuss the role of ectopic lipid accumulation in the liver. Secondly, we also summarize recent findings emphasizing the role of main inflammatory markers in both NAFLD and insulin resistance and their potential role in modulating hepatic fat content in NAFLD and associated hepatic insulin resistance.
Division of Metabolic and Vascular Health, Warwickshire Institute for the Study of Diabetes, Clinical Sciences Research Laboratories, Warwick Medical School, University Hospital Site, University of Warwick, Coventry CV2 2DX, UK
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Division of Metabolic and Vascular Health, Warwickshire Institute for the Study of Diabetes, Clinical Sciences Research Laboratories, Warwick Medical School, University Hospital Site, University of Warwick, Coventry CV2 2DX, UK
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Adipose tissue is an active endocrine organ, and our knowledge of this secretory tissue, in recent years, has led us to completely rethink how our body functions and becomes dysregulated with weight gain. Human adipose tissue appears to act as a multifunctional secretory organ with the capacity to control energy homoeostasis through peripheral and central regulation of energy homoeostasis. It also plays an important role in innate immunity. However, the capability to more than double its original mass to cope with positive energy balance in obesity leads to many pathogenic changes. These changes arise within the adipose tissue as well as inducing secondary detrimental effects on other organs like muscle and liver, including chronic low-grade inflammation mediated by adipocytokines (adipokine inflammation). This inflammation is modulated by dietary factors and nutrients including glucose and lipids, as well as gut bacteria in the form of endotoxin or LPS. The aim of this current review is to consider the impact of nutrients such as glucose and lipids on inflammatory pathways, specifically within adipose tissue. Furthermore, how nutrients such as these can influence adipokine inflammation and consequently insulin resistance directly through their effects on secretion of adipocytokines (TNFα, IL6 and resistin) as well as indirectly through increases in endotoxin is discussed.
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Exposure to tobacco smoke is related to changes in energy balance regulation and several endocrine dysfunctions. Previously, we showed that maternal nicotine (the main addictive compound of tobacco) exposure exclusively during lactation affects biochemical profiles in mothers, milk, and pups. As the possible consequences for mothers and offspring of maternal smoking during lactation are still unknown, we evaluated the effects of tobacco smoke exposure on nutritional, biochemical, and hormonal parameters in dams and pups at weaning. After 72 h from birth, lactating rats were divided into two groups: smoke-exposed (S) in a cigarette-smoking machine, 4×1 h per day throughout the lactation period without pups; control (C), rats were treated the same as the experimental group but exposed to filtered air. Dams and pups were killed at weaning (21 days of lactation). Body weight and food intake were evaluated. Milk, blood, visceral fat, adrenal, and carcass were collected. S dams showed hyperprolactinemia (+50%), hypoinsulinemia (−40%), hypoleptinemia (−46%), as well as lower triglycerides (−53%) and very low-density lipoprotein cholesterol (−50%). Milk of S dams had higher lactose (+52%) and triglycerides (+78%). S pups presented higher body protein (+17%), lower total (−24%) and subcutaneous fat contents (−25%), hypoglycemia (−11%), hyperinsulinemia (+28%), hypocorticosteronemia (−40%), lower adrenal catecholamine content (−40%), hypertriglyceridemia (+34%), higher high-density lipoprotein cholesterol (+16%), and lower low-density lipoprotein cholesterol (−45%). In conclusion, tobacco smoke exposure leads to changes in nutritional, biochemical, and hormonal parameters in dams and, passively through the milk, may promote several important metabolic disorders in the progeny.
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Analysis of knockout mice suggests that the neurotropin-inducible secreted polypeptide VGF (non-acronymic) plays an important role in the regulation of energy balance. VGF is synthesized by neurons in the central and peripheral nervous systems (CNS, PNS), as well as in the adult pituitary, adrenal medulla, endocrine cells of the stomach and pancreatic beta cells. Thus VGF, like cholecystokinin, leptin, ghrelin and other peptide hormones that have been shown to regulate feeding and energy expenditure, is synthesized in both the gut and the brain. Although detailed developmental studies of VGF localization in the CNS and PNS have been completed, little is known about the ontogeny of VGF expression in endocrine and neuroendocrine tIssues. Here, we report that VGF mRNA is detectable as early as embryonic day 15.5 in the developing rat gastrointestinal and esophageal lumen, pancreas, adrenal, and pituitary, and we further demonstrate that VGF mRNA is synthesized in the gravid rat uterus, together supporting possible functional roles for this polypeptide outside the nervous system and in the enteric plexus.
