Weight loss increases circulating levels of ghrelin in human obesity

Hansen, Troels Krarup; Dall, Rolf; Hosoda, Hiroshi; Kojima, Masayasu; Kangawa, Kenji; Christiansen, Jens Sandahl; Jørgensen, Jens Otto Lunde

doi:10.1046/j.0300-0664.2001.01456.x

Cited by 419 publications

(276 citation statements)

References 13 publications

Supporting

Mentioning

229

Contrasting

Unclassified

Order By: Relevance

“…Studies based on intensive energy restriction (very low caloric diet) showed increasing ghrelin concentrations. 13,14 In contrast to this, our study with high-carbohydrate and low-fat diet demonstrated no significant increase in ghrelin levels despite a small but not significant tendency (increase in ghrelin levels of 4%). Probably the kind of treatment to reduce weight may have influenced the ghrelin levels and may explain the different study results.…”

Section: Ghrelin In Obese Children T Reinehr Et Alcontrasting

confidence: 99%

“…9 In obese adults and children, leptin levels have shown to be increased, while ghrelin levels are decreased. 7,[9][10][11] There are only few studies consisting of only a small number of subjects, which analyze the changes in ghrelin levels due to reduction of overweight in a time period of weeks up to months with contradictory results: four studies reported increasing ghrelin levels, [12][13][14][15] four studies no changes of ghrelin levels [16][17][18][19] and one study decreasing ghrelin levels after weight reduction. 20 Until now, there is only one study on ghrelin levels in obese children after weight reduction.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ghrelin levels before and after reduction of overweight due to a low-fat high-carbohydrate diet in obese children and adolescents

et al. 2005

View full text Add to dashboard Cite

BACKGROUND: There are conflicting results for ghrelin changes in reduction of overweight. Increasing ghrelin levels in weight reduction are considered to be responsible for compensatory mechanisms that make the reduction of overweight unlikely to be sustained. METHODS:We have analyzed fasting serum ghrelin levels, weighed dietary record and, as biochemical markers of clinically relevant reduction of overweight, leptin, adiponectin and insulin levels and insulin resistance measured by homeostasis model assessment (HOMA) at baseline and after a 1-y outpatient weight reduction program based on a high-carbohydrate and low-fat diet in 37 obese children (median age 10 y). We divided these children into two subgroups according to their degree of weight loss (substantial reduction of overweight: decrease in SDS-BMIZ0.5). Furthermore, we analyzed ghrelin levels in 16 normalweight children. RESULTS: Obese children demonstrated significant (Po0.001) lower ghrelin levels compared to normal-weight children. Daily caloric intake (P ¼ 0.004) and percentage fat content decreased significantly (Po0.001), while percentage carbohydrate content increased significantly (P ¼ 0.003) between baseline and 1-y follow-up in the obese children. The substantial reduction of overweight in 16 children (median SDS-BMI ¼ À0.7) was associated with significant changes in insulin resistance (median decrease of HOMA 27%; P ¼ 0.013), insulin (median decrease 25%, P ¼ 0.036), adiponectin (median increase 15%; P ¼ 0.003), and leptin levels (median decrease 19%; P ¼ 0.023), while there were no significant changes in ghrelin levels (median increase 4%; P ¼ 0.326). In the 21 children without substantial reduction of overweight (median SDS-BMI ¼ À0.3), there were no significant changes in insulin resistance and in insulin, adiponectin, leptin and ghrelin levels. CONCLUSIONS: We conclude that in obese children, low-fat high-carbohydrate diet-induced weight loss does not change ghrelin secretion, but significantly decreases leptin levels, increases adiponectin levels and improves insulin resistance determined by significantly decreased insulin resistance indices as well as lowered serum insulin levels.

show abstract

Section: Ghrelin In Obese Children T Reinehr Et Alcontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ghrelin levels before and after reduction of overweight due to a low-fat high-carbohydrate diet in obese children and adolescents

et al. 2005

View full text Add to dashboard Cite

show abstract

“…Ghrelin is a 28-amino-acid peptide hormone produced mainly in the stomach fundus and is the most potent appetitestimulating hormone coming from the gastrointestinal tract [29]. Ghrelin is generally up-regulated under conditions of negative energy balance and down-regulated in the setting of positive energy balance; fasting serum ghrelin levels are usually low in obese subjects compared with lean individuals [30], and fasting plasma levels rise with diet induced weight loss [14,31]. Ghrelin was shown to increase food intake dose-dependently in lean and obese Zucker rats [32].…”

Section: Discussionmentioning

confidence: 99%

Increase in Ghrelin Levels After Weight Loss in Obese Zucker Rats is Prevented by Gastric Banding

et al. 2007

View full text Add to dashboard Cite

Background Gastric banding is thought to decrease appetite in addition to the mechanical effects of food restriction, although this has been difficult to demonstrate in human studies. Our aim was to investigate the changes in orexigenic signals in the obese Zucker rat after gastric banding. Methods Obese Zucker rats ( fa/fa) were submitted to gastric banding (GBP), sham gastric banding fed ad libitum (sham), or sham operation with food restriction, pair-fed to the gastric banding group (sham-PF). Lean Zucker rats ( fa/+) were used as additional controls. Body weight and food intake were daily recorded for 21 days after surgery when epididymal fat was weighed and fasting ghrelin and hypothalamic NPY mRNA expression were measured. Results Gastric banding in obese Zucker rats resulted in a significant decrease of cumulative body weight gain and food intake. Furthermore, gastric banded rats were leaner than Sham-PF, as expressed by a significantly lower epididymal fat weight. Ghrelin levels of gastric banded rats were not increased when compared to sham-operated animals fed ad libitum and were significantly lower than the levels of weight matched sham-PF rats (1116.9±103.3 g GBP vs 963.2±54.3 g sham, 3,079.5±221.6 sham-PF and 2,969.9±150.9 g lean rats, p<0.001); hypothalamic NPY mRNA expression was not increased in GBP when compared to sham-operated rats. Conclusion In obese Zucker rats, GBP prevents the increase in orexigenic signals that occur during caloric deprivation. Our data support the hypothesis that sustained weight loss observed after gastric banding does not depend solely on food restriction.

show abstract

“…Weight loss has been shown to induce an increase in ghrelin levels. 62 Moreover, it has been shown that ghrelin may decrease BP, improve endothelial function and inhibit vascular oxidative stress in spontaneously hypertensive rats. 63 The endocannabinoids represent polyunsaturated fatty-acid derivatives, which take part in a large neuromodulatory signaling system for the control of balance between food intake and satiation.…”

Section: Mechanisms Of Obesity-induced Hypertension V Kotsis Et Almentioning

confidence: 99%

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

Weight loss increases circulating levels of ghrelin in human obesity

Abstract: This study provides evidence of a reversible suppression of ghrelin associated with obesity. The feasibility of measuring ghrelin in the circulation provides a new tool for the investigation of the complex hormonal regulation of appetite and energy balance.

Cited by 419 publications

References 13 publications

Ghrelin levels before and after reduction of overweight due to a low-fat high-carbohydrate diet in obese children and adolescents

Ghrelin levels before and after reduction of overweight due to a low-fat high-carbohydrate diet in obese children and adolescents

Increase in Ghrelin Levels After Weight Loss in Obese Zucker Rats is Prevented by Gastric Banding

Mechanisms of obesity-induced hypertension

Contact Info

Product

Resources

About