Hypothalamic and genetic obesity in experimental animals: an autonomic and endocrine hypothesis.

Bray, George A.; York, David A.

doi:10.1152/physrev.1979.59.3.719

Cited by 1,155 publications

(613 citation statements)

References 84 publications

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“…Our data are similar to those reached with VMN lesion in original studies of Brobeck et al (1943) and Tepperman et al (1943) and, reproduced later by Bray and York (1979), Hallonquist and Brandes (1983) and Vilberg and Keesey (1984). It is known at moment that among multiple disturbances caused by VMN lesion one of them is the disconnection between peripheral signal of leptin and mRNA ex-pression of neuropeptide Y (NPY).…”

Section: Discussionsupporting

confidence: 91%

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A reassessment of the role of serotonergic system in the control of feeding behavior

Medeiros

Costa-e-Sousa

Olivares

et al. 2005

An. Acad. Bras. Ciênc.

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The role of serotonergic system in the feeding behavior was appraised by electrolytic lesions in the dorsal raphe nucleus (DRN) and administration of para-chlorophenylalanine (PCPA, 3 mg/5 µl, icv). Chronic evaluations were accomplished through 120 and 360 days in PCPA-injected and DRN-lesioned rats, respectively. Acute food intake was evaluated in fasted rats and submitted to injection of PCPA and hydroxytryptophan (LHTP, 30 mg/kg, ip). DRN-lesioned rats exhibited 22-80% increase in food intake up to sixth month, whereas the obesity was evident and sustained by whole period. In PCPA-injected rats was observed an initial increase in the food intake followed by hypophagy from 25 th to 30 th day and a transitory increase of body weight from 5 th to 60 th day. In the acute study, the LHTP reverted partially the PCPA-induced increase in food intake of fasted rats suggesting a sustained capacity of decarboxylation of precursor by serotonergic neurons. Slow restoration of the levels of food intake in DRN-lesioned rats reveals a neuroplasticity in the systems that regulate feeding behavior. A plateau on the body weight curve in lesioned rats possibly represents the establishment of a new and higher set point of energetic balance.

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Section: Discussionsupporting

confidence: 91%

“…In this respect our observations parallel with findings regarding lesion of hypothalamic ventromedial nucleus (VMN) , Bray and York 1979, Hallonquist and Brandes 1983, Vilberg and Keesey 1984. These authors referred an intense increase of the food ingestion associated with obesity for long time.…”

Section: Discussionsupporting

confidence: 89%

A reassessment of the role of serotonergic system in the control of feeding behavior

Medeiros

Costa-e-Sousa

Olivares

et al. 2005

An. Acad. Bras. Ciênc.

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“…Hypercortisolism which is common in genetically obese fa/fa rats and db/db and ob/ob mice, has also been reported in obese humans with insulin resistance. 14,15 However, studies have also suggested that elevated cortisol levels in obese individuals are related to increased body mass, increased turnover and/or changes in cortisol-binding globulin. 16 A blunted long-term response of adrenal glucocorticoid release has been reported in obesity.…”

Section: Hpa Axis Dysregulation In Obesity and Depressionmentioning

confidence: 99%

Approaching the shared biology of obesity and depression: the stress axis as the locus of gene–environment interactions

et al. 2006

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Obesity and depression are serious public health problems and also constitute cardiovascular disease risk factors. Research organizations have called for efforts to explore the interrelationship between obesity and depression. A useful starting point is the fact that in both disorders there is dysregulation of stress systems. We review molecular and clinical evidence indicating that the mediators of the stress response are a key locus for geneenvironment interactions in the shared biology of depression and obesity. Scientific milestones include translational paradigms such as mice knockouts, imaging and pharmacogenomic approaches that can identify new therapeutic strategies for those burdened by these two afflictions of contemporary civilization. Perspectives for the future are promising. Our ability to dissect the underpinnings of common and complex diseases with shared substrates will be greatly enhanced by the Genes and Environment Initiative, the emerging Large Scale Studies of Genes and Environment in Common Disease, and the UK Biobank Project.

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“…They are characterized by many abnormalities including hyperphagia, fasting hyperglycaemia, and hyperinsulinaemia. They have fewer insulin receptors and their tissues, particularly muscle, show a marked resistance to the normal metabolic actions of this hormone [1]. Obese mice have similar quantities of total body protein to lean mice [2].…”

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confidence: 99%

A histochemical and morphological study of skeletal muscle from obese hyperglycaemic ob/ob mice

almond

Enser

1984

Diabetologia

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Summary. The histochemical and morphological charactefis= tics of muscles from lean and obese hyperglycaemic ob/ob mice were compared to determine the nature of the low skeletal muscle mass of the latter: Gastrocnemius and biceps brachii muscles from obese ob/ob mice were significantly lighter than those from lean mice; whereas the weights of soleus muscles were not significantly different. The small mass of the biceps brachii muscle resulted from a decrease in diameter of the large glycolytic fast white and fast intermediate fibres and a reduction in the proportion of fast white fibres.The size and frequency of the more oxidative fast red fibres was not different. The histochemical appearance of all fibre types studied from muscles in obese mice was identical to equivalent fibres in lean mice. The fat content of muscles from obese mice was three times greater than in lean mice whereas muscle DNA concentration was similar.Key words: Obese mice, muscle size, fibre type, fibre number, diabetes.Obese hyperglycaemic mice with the ob/ob genome have been used extensively as a model for Type 2 (noninsulin-dependent) diabetes. They are characterized by many abnormalities including hyperphagia, fasting hyperglycaemia, and hyperinsulinaemia. They have fewer insulin receptors and their tissues, particularly muscle, show a marked resistance to the normal metabolic actions of this hormone [1]. Obese mice have similar quantities of total body protein to lean mice [2]. However, extra protein present in their enlarged adipose tissue, liver, and intestine disguises a lower content of skeletal muscle protein [3,4].The smaller amount of muscle could be due to a decrease in the number of muscle fibres, or a reduced volume per fibre, or both. If there were fewer fibres within the muscles of obese mice, it would indicate a difference in pre-natat development compared with lean mice since in mice the majority of muscle fibres are present at or soon after birth [5, 6]-On the other hand, a decrease in the post-natal growth of fibres would be compatible with the other reported metabolic defects in ob/ob mice. Insulin is probably the most important physiological factor regulating the overall protein balance in skeletal muscle [7] since k not only stimulates the uptake of amino-acids and protein synthesis, [8] but also inhibits protein degradation. It is conceivable, therefore, that the inherent resistance of muscles from obese mice to the anabolic effects of insulin [9,10] could facilitate a decrease in the post-natal growth of this tissue. Plasma corticosteroid levels are also elevated in ob/ob mice [11,12] and may cause accelerated protein degradation and diversion of amino-acids into excessive gluconeogenesis [13]. If these metabolic abnormalities in obese mice are responsible for their decreased skeletal muscle mass, one would predict that fast and slow phasic muscles would respond differently, since either st~eptozotocin-induced diabetes [14] or corticosteroid injections in rats [15] cause large glycolytic fibres and fast phasic musc...

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Hypothalamic and genetic obesity in experimental animals: an autonomic and endocrine hypothesis.

Cited by 1,155 publications

References 84 publications

A reassessment of the role of serotonergic system in the control of feeding behavior

A reassessment of the role of serotonergic system in the control of feeding behavior

Approaching the shared biology of obesity and depression: the stress axis as the locus of gene–environment interactions

A histochemical and morphological study of skeletal muscle from obese hyperglycaemic ob/ob mice

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