scholarly journals Relationship of plasma leptin to plasma insulin and adiposity in normal weight and overweight women: effects of dietary fat content and sustained weight loss.

1996 ◽  
Vol 81 (12) ◽  
pp. 4406-4413 ◽  
Author(s):  
P J Havel ◽  
S Kasim-Karakas ◽  
W Mueller ◽  
P R Johnson ◽  
R L Gingerich ◽  
...  
Keyword(s):  
Weight Loss ◽  
Dietary Fat ◽  
Plasma Insulin ◽  
Fat Content ◽  
Normal Weight ◽  
Overweight Women ◽  
Sustained Weight Loss ◽  
Plasma Leptin ◽  
Relationship Of

scholarly journals Regulation of plasma leptin in mice: influence of age, high-fat diet, and fasting

1997 ◽  
Vol 273 (1) ◽  
pp. R113-R120 ◽  
Author(s):  
B. Ahren ◽  
S. Mansson ◽  
R. L. Gingerich ◽  
P. J. Havel
Keyword(s):  
Body Weight ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Plasma Insulin ◽  
Plasma Concentrations ◽  
Age Groups ◽  
Fat Content ◽  
High Fat ◽  
Background Strain ◽  
Plasma Leptin

Mechanisms regulating circulating leptin are incompletely understood. We developed a radioimmunoassay for mouse leptin to examine the influence of age, dietary fat content, and fasting on plasma concentrations of leptin in the background strain for the ob/ob mouse, the C57BL/6J mouse. Plasma leptin increased with age [5.3 +/- 0.6 ng/ml at 2 mo (n = 23) vs. 14.2 +/- 1.6 ng/ml at 11 mo (n = 15), P < 0.001]. Across all age groups (2-11 mo, n = 160), log plasma leptin correlated with body weight (r = 0.68, P < 0.0001), plasma insulin (r = 0.38, P < 0.001), and amount of intra-abdominal fat (r = 0.90, P < 0.001), as revealed by magnetic resonance imaging. Plasma leptin was increased by a high-fat diet (58% fat for 10 mo) and reduced by fasting for 48 h. The reduction of plasma leptin was correlated with the reduction of plasma insulin (r = 0.43, P = 0.012) but not with the initial body weight or the change in body weight. Moreover, the reduction in plasma leptin by fasting was impaired by high-fat diet. Thus plasma leptin in C57BL/6J mice 1) increases with age or a high-fat diet; 2) correlates with body weight, fat content, and plasma insulin; and 3) is reduced during fasting by an action inhibited by high-fat diet and related to changes of plasma insulin.

scholarly journals Moderate Weight Loss Modifies Leptin and Ghrelin Synthesis Rhythms but Not the Subjective Sensations of Appetite in Obesity Patients

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 916
Author(s):  
Juan José Hernández Morante ◽  
Inmaculada Díaz Soler ◽  
Joaquín S. Galindo Muñoz ◽  
Horacio Pérez Sánchez ◽  
Mª del Carmen Barberá Ortega ◽  
...  
Keyword(s):  
Weight Loss ◽  
Dietary Intervention ◽  
Physiological Function ◽  
Normal Weight ◽  
Ghrelin Level ◽  
Physiological Signals ◽  
Daily Rhythms ◽  
The Mean ◽  
Daily Variability ◽  
Plasma Leptin

Obesity is characterized by a resistance to appetite-regulating hormones, leading to a misalignment between the physiological signals and the perceived hunger/satiety signal. A disruption of the synthesis rhythm may explain this situation. The aim of this study was to evaluate the effect of dietary-induced weight loss on the daily rhythms of leptin and ghrelin and its influence on the daily variability of the appetite sensations of patients with obesity. Twenty subjects with obesity underwent a hypocaloric dietary intervention for 12 weeks. Plasma leptin and ghrelin were analyzed at baseline and at the end of the intervention and in 13 normal-weight controls. Appetite ratings were analyzed. Weight loss decreased leptin synthesis (pauc < 0.001) but not the rhythm characteristics, except the mean variability value (pmesor = 0.020). By contrast, the mean ghrelin level increased after weight loss. The rhythm characteristics were also modified until a rhythm similar to the normal-weight subjects was reached. The amount of variability of leptin and ghrelin was correlated with the effectiveness of the dietary intervention (p < 0.020 and p < 0.001, respectively). Losing weight partially restores the daily rhythms of leptin and modifies the ghrelin rhythms, but appetite sensations are barely modified, thus confirming that these hormones cannot exercise their physiological function properly.

scholarly journals Macronutrient balances and obesity: the role of diet and physical activity

1999 ◽  
Vol 2 (3a) ◽  
pp. 341-347 ◽  
Author(s):  
Arne Astrup
Keyword(s):  
Physical Activity ◽  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Physical Fitness ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Fat Oxidation ◽  
Fat Content ◽  
High Fat

AbstractObservational cross-sectional and longitudinal studies suggest that a high fat diet and physical inactivity are independent risk factors for weight gain and obesity. Mechanistic and intervention studies support that fat possesses a lower satiating power than carbohydrate and protein, and a diet low in fat therefore decreases energy intake. The effect of dietary fat on energy balance is enhanced in susceptible subjects, particularly in sedentary individuals with a genetic predisposition to obesity who consume a high fat diet.Dietary carbohydrate promotes its own oxidation by an insulin-mediated stimulation of glucose oxidation. In contrast, high fat meals do not increase fat oxidation acutely. A sedentary life-style and low physical fitness cause a low muscular fat oxidation capacity, and the consumption of a high fat diet by these individuals promotes fat storage in a synergistic fashion.Ad libitum low fat diets cause weight loss proportional to pre-treatment body weight in a dose-dependent way, i.e. weight loss is correlated positively to the reduction in dietary fat content. Increased physical activity prevents relapse after weight loss and studies have shown that those who keep up a higher level of physical activity are more successful in maintaining the reduced body weight. In conclusion, important interactions exist between genetic make up, dietary fat and physical fitness, so that a low fitness level and susceptible genes reduce muscular fat oxidation capacity which may decrease the tolerance of dietary fat. Increasing daily physical activity and reducing dietary fat content may be more effective when combined than when separate in preventing weight gain and obesity.

Altered expression of type 2 CRH receptor mRNA in the VMH by glucocorticoids and starvation

1998 ◽  
Vol 275 (4) ◽  
pp. R1138-R1145 ◽  
Author(s):  
Shinya Makino ◽  
Mitsuru Nishiyama ◽  
Koichi Asaba ◽  
Philip W. Gold ◽  
Kozo Hashimoto
Keyword(s):  
Weight Loss ◽  
Food Intake ◽  
Plasma Insulin ◽  
High Dose ◽  
Mrna Levels ◽  
Experimental Conditions ◽  
Altered Expression ◽  
Plasma Leptin ◽  
The Impact

In the rat, high-dose corticosterone (Cort) administration, the hypercortisolism of starvation, and adrenalectomy are all associated with decreased food intake and weight loss. We report here a study of the effects of high-dose Cort administration, starvation, and adrenalectomy on two peripheral hormones known to influence food intake and energy use, insulin and leptin. We also studied the impact of these interventions on the levels of type 2 corticotropin-releasing hormone receptor (CRHR-2) mRNA in the hypothalamic paraventricular nucleus (PVN) and ventromedial hypothalamus (VMH). The VMH is classically referred to as the satiety center because electrical stimulation of the VMH leads to inhibition of food intake, whereas CRHR-2 are thought to transduce the profound anorexogenic effects of CRH or its related peptide urocortin. Starvation and adrenalectomy each lowered plasma insulin and leptin levels and were associated with decrements in CRHR-2 mRNA levels in the VMH. Cort administration increased plasma leptin levels profoundly, as well as plasma insulin levels and the levels of VMH CRHR-2 mRNA. Under all experimental conditions, a positive correlation was seen between plasma leptin levels and VMH CRHR-2 mRNA. These data suggest that decreased food intake and weight loss after high-dose Cort administration at least partially depend on the profound impact of Cort on plasma leptin secretion in the rat; they suggest, moreover, an additional mechanism for the satiety-inducing effects of leptin, namely increasing CRHR-2 in the VMH. The concordance of a fall in plasma insulin and leptin levels with the fall in VMH CRHR-2 mRNA levels further supports the idea that compensatory responses during starvation and adrenalectomy include not only the disinhibiting effects of reduced insulin and leptin levels on appetite through already-described mechanisms but also via an effect of leptin on VMH CRHR-2. Neither Cort administration, starvation, nor adrenalectomy influenced the levels of CRHR-2 mRNA in the PVN, suggesting that these receptors are differentially regulated in different hypothalamic regions.

Relationship of dietary fat content to food preferences in young rats

1990 ◽  
Vol 48 (5) ◽  
pp. 581-586 ◽  
Author(s):  
Zoe S. Warwick ◽  
Susan S. Schiffman ◽  
John J.B. Anderson
Keyword(s):  
Dietary Fat ◽  
Food Preferences ◽  
Fat Content ◽  
Young Rats ◽  
Relationship Of

scholarly journals Marked and rapid decreases of circulating leptin in streptozotocin diabetic rats: reversal by insulin

1998 ◽  
Vol 274 (5) ◽  
pp. R1482-R1491 ◽  
Author(s):  
Peter J. Havel ◽  
Janet Y. Uriu-Hare ◽  
Tina Liu ◽  
Kimber L. Stanhope ◽  
Judith S. Stern ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Subcutaneous Insulin ◽  
Glucose Lowering ◽  
Streptozotocin Diabetic Rats ◽  
Plasma Leptin

Evidence for regulation of circulating leptin by insulin is conflicting. Diabetes was induced in rats with streptozotocin (STZ; 40 mg ⋅ kg−1⋅ day−1× 2 days) to examine the effect of insulin-deficient diabetes and insulin treatment on circulating leptin. After 12 wk, plasma leptin concentrations in untreated rats were all <0.4 ng/ml versus 4.9 ± 0.9 ng/ml in control animals ( P < 0.005). In rats treated with subcutaneous insulin implants for 12 wk, which reduced hyperglycemia by ∼50%, plasma leptin was 2.1 ± 0.6 ng/ml, whereas leptin concentrations were 6.0 ± 1.6 ng/ml in insulin-implanted rats receiving supplemental injections of insulin for 4 days to normalize plasma glucose ( P< 0.005 vs. STZ untreated). In a second experiment, plasma leptin was monitored at biweekly intervals during 12 wk of diabetes. In rats treated with insulin implants, plasma leptin concentrations were inversely proportional to glycemia ( r= −0.64; P < 0.0001) and unrelated to body weight ( P = 0.40). In a third experiment, plasma leptin concentrations were examined very early after the induction of diabetes. Within 24 h after STZ injection, plasma insulin decreased from 480 ± 30 to 130 ± 10 pM ( P < 0.0001), plasma glucose increased from 7.0 ± 0.2 to 24.8 ± 0.5 mM, and plasma leptin decreased from 3.2 ± 0.2 to 1.2 ± 0.1 ng/ml (Δ = −63 ± 3%, P < 0.0001). In a subset of diabetic rats treated with insulin for 2 days, glucose decreased to 11.7 ± 3.9 mM and leptin increased from 0.5 ± 0.1 to 2.9 ± 0.6 ng/ml ( P< 0.01) without an effect on epididymal fat weight. The change of leptin was correlated with the degree of glucose lowering ( r = 0.75, P < 0.05). Thus insulin-deficient diabetes produces rapid and sustained decreases of leptin that are not solely dependent on weight loss, whereas insulin treatment reverses the hypoleptinemia. We hypothesize that decreased glucose transport into adipose tissue may contribute to decreased leptin production in insulin-deficient diabetes.

scholarly journals Roles of Leptin and Ghrelin in the Loss of Body Weight Caused by a Low Fat, High Carbohydrate Diet

2003 ◽  
Vol 88 (4) ◽  
pp. 1577-1586 ◽  
Author(s):  
David S. Weigle ◽  
David E. Cummings ◽  
Patricia D. Newby ◽  
Patricia A. Breen ◽  
R. Scott Frayo ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Dietary Fat ◽  
Human Subjects ◽  
Energy Restriction ◽  
Low Fat ◽  
Time Curve ◽  
Dietary Energy Restriction ◽  
Ad Libitum ◽  
Plasma Leptin

Loss of body fat by caloric restriction is accompanied by decreased circulating leptin levels, increased ghrelin levels, and increased appetite. In contrast, dietary fat restriction often decreases adiposity without increasing appetite. Substitution of dietary carbohydrate for fat has been shown to increase the area under the plasma leptin vs. time curve (AUC) over the course of 24 h. This effect, if sustained, could explain the absence of a compensatory increase in appetite on a low fat diet. To clarify the effect of dietary fat restriction on leptin and ghrelin, we measured AUC for these hormones in human subjects after each of the following sequential diets: 2 wk on a weight-maintaining 35% fat (F), 45% carbohydrate (C), 20% protein (P) diet (n = 18); 2 wk on an isocaloric 15% F, 65% C, 20% P diet (n = 18); and 12 wk on an ad libitum 15% F, 65% C, 20% P diet (n = 16). AUC for leptin was similar on the isocaloric 15% F and 35% F diets (555 ± 57 vs. 580 ± 56 ng/ml·24 h; P = NS). Body weight decreased from 74.6 ± 2.4 to 70.8 ± 2.7 kg on the ad libitum 15% F diet (P &lt; 0.001) without compensatory increases in food consumption or AUC for ghrelin. Proportional amplitude of the 24-h leptin profile was increased after 12 wk on the 15% fat diet. We conclude that weight loss early in the course of dietary fat restriction occurs independently of increased plasma leptin levels, but that a later increase in amplitude of the 24-h leptin signal may contribute to ongoing weight loss. Fat restriction avoids the increase in ghrelin levels caused by dietary energy restriction.

Dietary Fat Intake, Supplements, and Weight Loss

2000 ◽  
Vol 25 (6) ◽  
pp. 495-523 ◽  
Author(s):  
David J. Dyck
Keyword(s):  
Weight Loss ◽  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Dietary Fat ◽  
Fat Oxidation ◽  
Fat Content ◽  
High Fat ◽  
Underlying Assumption ◽  
High Fat Diets ◽  
Fat Diets

Although there remains controversy regarding the role of macronutrient balance in the etiology of obesity, the consumption of high-fat diets appears to be strongly implicated in its development. Evidence that fat oxidation does not adjust rapidly to acute increases in dietary fat, as well as a decreased capacity to oxidize fat in the postprandial state in the obese, suggest that diets high in fat may lead to the accumulation of fat stores. Novel data is also presented suggesting that in rodents, high-fat diets may lead to the development of leptin resistance in skeletal muscle and subsequent accumulations of muscle triacylglycerol. Nevertheless, several current fad diets recommend drastically reduced carbohydrate intake, with a concurrent increase in fat content. Such recommendations are based on the underlying assumption that by reducing circulating insulin levels, lipolysis and lipid oxidation will be enhanced and fat storage reduced. Numerous supplements are purported to increase fat oxidation (carnitine, conjugated linoleic acid), increase metabolic rate (ephedrine, pyruvate), or inhibit hepatic lipogenesis (hydroxycitrate). All of these compounds are currently marketed in supplemental form to increase weight loss, but few have actually been shown to be effective in scientific studies. To date, there is little or no evidence supporting that carnitine or hydroxycitrate supplementation are of any value for weight loss in humans. Supplements such as pyruvate have been shown to be effective at high dosages, but there is little mechanistic information to explain its purported effect or data to indicate its effectiveness at lower dosages. Conjugated linoleic acid has been shown to stimulate fat utilization and decrease body fat content in mice but has not been tested in humans. The effects of ephedrine, in conjunction with methylxanthines and aspirin, in humans appears unequivocal but includes various cardiovascular side effects. None of these compounds have been tested for their effectiveness or safety over prolonged periods of time. Key words: carnitine, conjugated linoleic acid, ephedrine, pyruvate, hydroxycitrate

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