Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake

Denis, Raphaël; Chen, Bing; Brocklehurst, Sarah; Harrold, Joanne A.; Vernon, Richard G.; Williams, Gareth

doi:10.1677/joe.1.05659

Cited by 23 publications

(14 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, overexpression of the suppressor of cytokine signaling 3 by high-circulating leptin, which serves as a feedback mechanism, has been suggested to have a function in the pathogenesis of leptin resistance. 52 The close relationship of hyperleptinemia with hypertension is further supported by observations obtained in obese leptin-deficiency mice, which are obese, but do not exhibit hypertension. Obesity does not invariably increase BP in mice and probably also in human beings and the arterial pressure response to obesity may depend critically on the underlying genetic and neuroendocrine mechanisms.…”

Section: Function Of Hormones Insulinmentioning

confidence: 78%

Mechanisms of obesity-induced hypertension

et al. 2010

View full text Add to dashboard Cite

The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies. Hypertension Research (2010) 33, 386-393; doi:10.1038/hr.2010.9Keywords: leptin; obesity; pressure natriuresis; rennin-angiotensin-aldosterone system; sympathetic nervous system INTRODUCTION Obesity is a common disorder that develops from the interaction between the genotype and the environment and involves social, behavioral, cultural, physiological, metabolic and genetic factors. A large number of studies have shown that obesity has an important negative impact on health in a population, leading to the recommendation for general practitioners to have an important function in the management of this condition and of its associated comorbidities such as hypertension, hyperlipidemia and hyperinsulinemia/insulin resistance. The relationship between obesity and hypertension is well established both in adults and children. 1,2 Obese individuals exhibit higher levels of office as well as ambulatory blood pressure (BP) from childhood to old age. Obese subjects display higher BP levels than non-obese individuals even in the normotensive range. The combination of obesity, hypertension and other cardiovascular risk factors significantly increases the probability of adverse cardiovascular outcomes, and raises considerations for aggressive treatment strategies. 3 The mechanisms through which obesity directly causes hypertension are still an area of research. Human and animal studies have elucidated the function of adipose tissue derivatives (adipokines and cytokines), neurohumoral pathways, metabolic functions and modulation of pressor/depressor mechanisms. Although obesity-related hypertension may be the result of a combinatio...

show abstract

Section: Function Of Hormones Insulinmentioning

confidence: 78%

Mechanisms of obesity-induced hypertension

et al. 2010

View full text Add to dashboard Cite

show abstract

“…The influence of the length of day on SOCS-3 transcription has also been observed in bovine mammary glands (Wall et al 2005). Moreover, diurnal changes in the synthesis of SOCS have been observed in the rat brain (Denis et al 2004).…”

Section: Introductionmentioning

confidence: 79%

Seasonal effects of central leptin infusion and prolactin treatment on pituitary SOCS-3 gene expression in ewes

Szczęsna

Zieba²,

Klocek-Gorka³

et al. 2010

Journal of Endocrinology

View full text Add to dashboard Cite

Suppressors of cytokine signalling (SOCS) negatively regulate cytokine-induced signalling pathways and may be involved in leptin and prolactin (PRL) interactions. Herein, we examined the effect of PRL on SOCS-3 mRNA expression in pituitary explants and investigated whether leptin could modify the expression of SOCS-3 mRNA in pituitary explants. In the first experiment, we used pituitaries isolated from 16 ewes decapitated in March, May, July and October (four per month). Tissues were cut into 50 mg explants, which were treated with control or medium containing PRL (100 or 300 ng/ml). Incubation was maintained for different time intervals: 0, 60, 120, 180, 240 or 300 min. Real-time PCR was used to measure SOCS-3 mRNA levels. In the second study, we used 24 ewes surgically fitted with third ventricle cannulas (12 were used during the long-day period, and 12 were used during the short-day (SD) period). Each ewe was administered an i.c.v. injection of Ringer-Locke buffer or leptin (0 . 5 or 1 . 0 mg/kg body weight). Explants of anterior pituitaries were collected and snap frozen 1 h after injection. Semiquantitative expression of SOCS-3 mRNA was performed using reverse transcription-PCR. PRL stimulated SOCS-3 expression in the pituitaries collected in March (P!0 . 05) and May (P!0 . 01 and P!0 . 05 for lower and higher doses respectively), inhibited SOCS-3 expression in pituitaries collected in July (P!0 . 01) and had no effect in pituitaries collected in October. Treatment with leptin increased SOCS-3 expression during the SDs in a dose-dependent manner (P!0 . 01). The results demonstrated that photoperiod may be involved in leptin and PRL effects on SOCS-3 expression in sheep.

show abstract

“…In lactating low-protein dams the insulinemia reduced in 2-thirds as compared to control lactating, prompting to a higher release of fatty acids. According to Sipols et al [32], low insulin and leptin concentrations can lead to hyperphagia, which could have contributed to the elevation of food intake verified in both lactating groups [6, 33]. …”

Section: Discussionmentioning

confidence: 99%

Low-Protein Diet during Lactation and Maternal Metabolism in Rats

Moretto

Ballen

Gonçalves

et al. 2011

ISRN Obstetrics and Gynecology

View full text Add to dashboard Cite

Some metabolic alterations were evaluated in Wistar rats which received control or low-protein (17%; 6%) diets, from the pregnancy until the end of lactation: control non-lactating (CNL), lactating (CL), low-protein non-lactating (LPNL) and lactating (LPL) groups. Despite the increased food intake by LPL dams, both LP groups reduced protein intake and final body mass was lower in LPL. Higher serum glucose occurred in both LP groups. Lactation induced lower insulin and glucagon levels, but these were reduced by LP diet. Prolactin levels rose in lactating, but were impaired in LPL, followed by losses of mammary gland (MAG) mass and, a fall in serum leptin in lactating dams. Lipid content also reduced in MAG and gonadal white adipose tissue of lactating and, in LPL, contributed to a decreased daily milk production, and consequent impairment of body mass gain by LPL pups. Liver mass, lipid content and ATP-citrate enzyme activity were increased by lactation, but malic enzyme and lipid: glycogen ratio elevated only in LPL. Conclusion. LP diet reduced the development of MAG and prolactin secretion which compromised milk production and pups growth. Moreover, this diet enhanced the store of lipid to glycogen ratio and suggests a higher risk of fatty liver development.

show abstract

Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake

Cited by 23 publications

References 53 publications

Mechanisms of obesity-induced hypertension

Mechanisms of obesity-induced hypertension

Seasonal effects of central leptin infusion and prolactin treatment on pituitary SOCS-3 gene expression in ewes

Low-Protein Diet during Lactation and Maternal Metabolism in Rats

Contact Info

Product

Resources

About