Pancreatic growth and enzyme profiles in weanling rats with normophagic hypothalamic obesity

1984 ◽  
Vol 62 (12) ◽  
pp. 1533-1538 ◽  
Author(s):  
Lee L. Bernardis ◽  
Ping C. Lee ◽  
Stephen Brooks ◽  
Emanuel Lebenthal
Keyword(s):  
Male Rats ◽  
Hypothalamic Nucleus ◽  
Hypothalamic Obesity ◽  
Pancreatic Growth ◽  
Ventromedial Hypothalamic Nucleus ◽  
Weanling Rats ◽  
Normal Body Weight ◽  
And Control ◽  
Enzyme Changes

Weanling male rats with ventromedial hypothalamic lesions (VMNL rats) and sham-operated controls were killed 1, 2, 4, and 5 weeks postoperatively. The VMNL rats developed normophagic hypothalamic obesity in the presence of normal body weight and reduced linear growth. In both VMNL and control rats, pancreatic weight and protein content increased with time but were lower in the lesioned animals. Pancreatic DNA content was arrested in VMNL rats and remained so during the remainder of the experiment. The only significant enzyme changes (trypsinogen, amylase, and lipase) were evident in higher trypsinogen concentration in VMNL rats during 2 and 4 weeks after lesion production. In view of previous data on both hypophysectomized and VMNL rats and the known role of the ventromedial hypothalamic nucleus in neuroendocrine and neuroautonomic function, it is speculated that the changes observed here are in part due to disruption of neuroendocrine and in part due to disturbance of neuroautonomic control systems.

scholarly journals Knockout Mice Lacking Steroidogenic Factor 1 Are a Novel Genetic Model of Hypothalamic Obesity

Endocrinology ◽  
2002 ◽  
Vol 143 (2) ◽  
pp. 607-614 ◽  
Author(s):  
Gregor Majdic ◽  
Morag Young ◽  
Elise Gomez-Sanchez ◽  
Paul Anderson ◽  
Lidia S. Szczepaniak ◽  
...  
Keyword(s):  
Genetic Model ◽  
Late Onset ◽  
Ventromedial Hypothalamus ◽  
Hypothalamic Nucleus ◽  
Weight Regulation ◽  
Wild Type ◽  
Hypothalamic Obesity ◽  
Steroidogenic Factor 1 ◽  
Ventromedial Hypothalamic Nucleus

Abstract Knockout (KO) mice lacking steroidogenic factor 1 (SF-1) exhibit a phenotype that includes adrenal and gonadal agenesis, impaired gonadotropin expression, and abnormalities of the ventromedial hypothalamic nucleus (VMH). Studies in rodents with lesions of the ventromedial hypothalamus have implicated the VMH in body weight regulation, suggesting that SF-1 KO mice may provide a genetic model of obesity. To prevent death, SF-1 KO mice were rescued with corticosteroid injections, followed by syngeneic adrenal transplants from wild-type (WT) littermates. Corticosterone and ACTH levels in WT and SF-1 KO mice were indistinguishable, documenting restoration of hypothalamic-pituitary-adrenal function. Although weights at earlier ages did not differ significantly from WT littermates, SF-1 KO mice were significantly heavier by 8 wk of age and eventually weighed almost twice as much as WT controls. Obesity in SF-1 KO mice predominantly resulted from decreased activity rather than increased food intake. Leptin was increased markedly, insulin was modestly elevated, and glucose was indistinguishable from WT mice. Although sex steroids in rodents affect weight, ovariectomy did not abolish the weight difference between WT and SF-1 KO mice. These SF-1 KO mice are a genetic model of late-onset obesity that may help elucidate the role of the VMH in weight regulation.

Cloning and sequence analysis of the human gene encoding steroidogenic factor 1

1996 ◽  
Vol 17 (2) ◽  
pp. 139-147 ◽  
Author(s):  
M Wong ◽  
M S Ramayya ◽  
G P Chrousos ◽  
P H Driggers ◽  
K L Parker
Keyword(s):  
Gonadal Development ◽  
Hypothalamic Nucleus ◽  
Endocrine Disorders ◽  
Orphan Nuclear Receptor ◽  
Gene Encoding ◽  
Steroidogenic Factor 1 ◽  
Ventromedial Hypothalamic Nucleus ◽  
And Function ◽  
Steroid Hydroxylases

ABSTRACT The orphan nuclear receptor steroidogenic factor 1 (SF-1) plays key roles in endocrine development and function. Initially identified as a positive regulator of the cytochrome P450 steroid hydroxylases, analyses of knockout mice deficient in SF-1 revealed that SF-1 is essential for adrenal and gonadal development, pituitary gonadotropin expression and formation of the ventromedial hypothalamic nucleus. Although more limited in scope, analyses of SF-1 in humans similarly have suggested that SF-1 is important for differentiated function in adrenocortical and gonadotrope adenomas. In the hope of extending our understanding of SF-1 function by identifying possible roles of SF-1 in clinical endocrine disorders, we isolated the FTZ-F1 gene encoding human SF-1 and mapped it to chromosome 9q33. In this report, we characterize the sequence and structural organization of the human cDNA and gene encoding SF-1, providing new insights into comparative aspects of SF-1 structure that will facilitate efforts to study the role of this transcription factor in human endocrine disorders.

scholarly journals Selective Loss of Leptin Receptors in the Ventromedial Hypothalamic Nucleus Results in Increased Adiposity and a Metabolic Syndrome

Endocrinology ◽  
2008 ◽  
Vol 149 (5) ◽  
pp. 2138-2148 ◽  
Author(s):  
Nathan C. Bingham ◽  
Kimberly K. Anderson ◽  
Anne L. Reuter ◽  
Nancy R. Stallings ◽  
Keith L. Parker
Keyword(s):  
Metabolic Syndrome ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Artificial Chromosome ◽  
Hypothalamic Nucleus ◽  
Steroidogenic Factor 1 ◽  
Low Fat Diet ◽  
Ventromedial Hypothalamic Nucleus

Leptin, an adipocyte-derived hormone, has emerged as a critical regulator of energy homeostasis. The leptin receptor (Lepr) is expressed in discrete regions of the brain; among the sites of highest expression are several mediobasal hypothalamic nuclei known to play a role in energy homeostasis, including the arcuate nucleus, the ventromedial hypothalamic nucleus (VMH), and the dorsomedial hypothalamic nucleus. Although most studies have focused on leptin’s actions in the arcuate nucleus, the role of Lepr in these other sites has received less attention. To explore the role of leptin signaling in the VMH, we used bacterial artificial chromosome transgenesis to target Cre recombinase to VMH neurons expressing steroidogenic factor 1, thereby inactivating a conditional Lepr allele specifically in steroidogenic factor 1 neurons of the VMH. These knockout (KO) mice, designated Lepr KOVMH, exhibited obesity, particularly when challenged with a high-fat diet. On a low-fat diet, Lepr KOVMH mice exhibited significantly increased adipose mass even when their weights were comparable to wild-type littermates. Furthermore, these mice exhibited a metabolic syndrome including hepatic steatosis, dyslipidemia, and hyperleptinemia. Lepr KOVMH mice were hyperinsulinemic from the age of weaning and eventually developed overt glucose intolerance. These data define nonredundant roles of the Lepr in VMH neurons in energy homeostasis and provide a model system for studying other actions of leptin in the VMH.

scholarly journals Lateral hypothalamus involvement in control of stress response by bed nucleus of the stria terminalis endocannabinoid neurotransmission in male rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lucas Gomes-de-Souza ◽  
Willian Costa-Ferreira ◽  
Michelle M. Mendonça ◽  
Carlos H. Xavier ◽  
Carlos C. Crestani
Keyword(s):  
Receptor Antagonist ◽  
Lateral Hypothalamus ◽  
Physiological Responses ◽  
Cardiovascular Responses ◽  
Male Rats ◽  
Hypothalamic Nucleus ◽  
Stria Terminalis ◽  
Gabaergic Neurotransmission ◽  
Bed Nucleus

AbstractThe endocannabinoid neurotransmission acting via local CB1 receptor in the bed nucleus of the stria terminalis (BNST) has been implicated in behavioral and physiological responses to emotional stress. However, the neural network related to this control is poorly understood. In this sense, the lateral hypothalamus (LH) is involved in stress responses, and BNST GABAergic neurons densely innervate this hypothalamic nucleus. However, a role of BNST projections to the LH in physiological responses to stress is unknown. Therefore, using male rats, we investigated the role of LH GABAergic neurotransmission in the regulation of cardiovascular responses to stress by CB1 receptors within the BNST. We observed that microinjection of the selective CB1 receptor antagonist AM251 into the BNST decreased the number of Fos-immunoreactive cells within the LH of rats submitted to acute restraint stress. Treatment of the BNST with AM251 also enhanced restraint-evoked tachycardia. Nevertheless, arterial pressure increase and sympathetically-mediated cutaneous vasoconstriction to restraint was not affected by CB1 receptor antagonism within the BNST. The effect of AM251 in the BNST on restraint-evoked tachycardia was abolished in animals pretreated with the selective GABAA receptor antagonist SR95531 in the LH. These results indicate that regulation of cardiovascular responses to stress by CB1 receptors in the BNST is mediated by GABAergic neurotransmission in the LH. Present data also provide evidence of the BNST endocannabinoid neurotransmission as a mechanism involved in LH neuronal activation during stressful events.

Dissociative analysis of ventromedial hypothalamic obesity syndrome

1990 ◽  
Vol 259 (4) ◽  
pp. R829-R835 ◽  
Author(s):  
W. L. Parkinson ◽  
H. P. Weingarten
Keyword(s):  
Ventromedial Hypothalamus ◽  
Hypothalamic Nucleus ◽  
Restricted Feeding ◽  
Hypothalamic Obesity ◽  
Ventromedial Hypothalamic Nucleus ◽  
Excessive Weight ◽  
Sham Surgery ◽  
Electrolytic Lesions ◽  
Ad Libitum ◽  
Obesity Syndrome

Electrolytic lesions of the ventromedial hypothalamus (VMH) produce an obesity syndrome characterized by hyperphagia, adiposity, and heightened parasympathetic tone. Experiments were conducted to evaluate the possibility that these symptoms arise from damage to distinct and separated loci within the hypothalamus. Rats received either VMH lesions, perifornical hypothalamic (PFH) knife cuts, ventromedial hypothalamic nucleus (VMN) lesions, or sham surgery (Sham). When maintained ad libitum, VMH and PFH rats were hyperphagic, overweight, and became obese. VMN rats were not hyperphagic, nor did they gain excessive weight, but they did develop an obesity reflected as a significantly elevated level of carcass fat. Under restricted feeding conditions, both VMH and VMN rats became obese; PFH rats did not. Also, only VMH lesions and PFH knife cuts increased basal gastric acid secretion. These data demonstrate dissociations between hyperphagia and obesity, as well as between stomach secretion and obesity, in the VMH syndrome. The implications of these findings for a dissociative model of the VMH obesity syndrome are discussed.

Moringa oleifera seed oil partially abrogates 2,3-dichlorovinyl dimethyl phosphate (Dichlorvos)-induced cardiac injury in rats: evidence for the role of oxidative stress

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Waid A. Saka ◽  
Titilayo E. Ayoade ◽  
Tunmise M. Akhigbe ◽  
Roland E. Akhigbe
Keyword(s):  
Moringa Oleifera ◽  
Seed Oil ◽  
Cardiac Tissue ◽  
Body Weight Gain ◽  
Cardiac Injury ◽  
Male Rats ◽  
Dimethyl Phosphate ◽  
Group B ◽  
And Control

AbstractObjectivesCardiovascular diseases are major causes of non-infectious diseases globally. The use of pesticides has been linked with the high global burden of non-communicable diseases. Despite the indiscriminate exposure to dichlorvos (DDVP) by inhalation, no report exists on its possible cardiotoxic effect. This study investigated the cardiotoxicity of DDVP exposure by inhalation and the possible role of Moringa oleifera seed oil.MethodsTwenty-one male rats were randomly assigned into 3 groups. Group A (control) received only standard rat diet and water ad’ libitum, group B (DDVP) was exposed to DDVP via inhalation for 15 min daily in addition to rat diet and water, and group C (DDVP + M. oleifera seed oil) received treatment as group B as well as 300 mg/kg of M. oleifera seed oil p.o for 28 days.ResultsSignificant reductions in body weight gain and cardiac weight were observed in DDVP-exposed animals (p<0.05). Similarly, 28 days of exposure to DDVP led to a significant increase in lactate dehydrogenase, creatinine kinase and troponin (p<0.05). DDVP-exposed rats also showed a significant increase in malondialdehyde, and a significant decline in superoxide dismutase and glutathione peroxidase (p<0.05). However, catalase was comparable in DDVP-exposed and control rats. Histopathological observations of the cardiac tissue revealed that DDVP caused marked fat degeneration and necrosis of the myocardial layer. The changes in DDVP-exposed rats were significantly, though not completely, restored by M. oleifera seed oil administration.ConclusionsThis study provides novel mechanistic information on the cardiotoxicity of DDVP inhalation, and the antioxidant potential of M. oleifera seed oil.

Morphogenesis of a New Human Herpes-Type Virus Isolate (Sasha Virus)

1973 ◽  
Vol 31 ◽  
pp. 592-593
Author(s):  
R. F. Zeigel ◽  
W. Munyon
Keyword(s):  
Virus Isolate ◽  
Calf Serum ◽  
Uranyl Acetate ◽  
Human Herpes ◽  
Human Embryonic Lung ◽  
Human Herpes Virus ◽  
Intracytoplasmic Inclusions ◽  
Hel Cells ◽  
And Control

In continuing studies on the role of viruses in biochemical transformation, Dr. Munyon has succeeded in isolating a highly infectious human herpes virus. Fluids of buccal pustular lesions from Sasha Munyon (10 mo. old) uiere introduced into monolayer sheets of human embryonic lung (HEL) cell cultures propagated in Eagles’ medium containing 5% calf serum. After 18 hours the cells exhibited a dramatic C.P.E. (intranuclear vacuoles, peripheral patching of chromatin, intracytoplasmic inclusions). Control HEL cells failed to reflect similar changes. Infected and control HEL cells were scraped from plastic flasks at 18 hrs. of incubation and centrifuged at 1200 × g for 15 min. Resultant cell packs uiere fixed in Dalton's chrome osmium, and post-fixed in aqueous uranyl acetate. Figure 1 illustrates typical hexagonal herpes-type nucleocapsids within the intranuclear virogenic regions. The nucleocapsids are approximately 100 nm in diameter. Nuclear membrane “translocation” (budding) uias observed.

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