No acute response of leptin to an oral fat load in obese patients and during circadian rhythm in healthy controls

Abstract

This study was done to elucidate the relationship between postprandial leptin and obesity, and the possible influence of the circadian rhythm on the dynamic leptin response to an oral fat load (OFLT). In experiment 1, we measured the leptin and insulin responses to an oral fat load in 16 non-diabetic obese subjects and in 16 healthy controls, matched for age and gender. In experiment 2, we measured the leptin and insulin responses to an OFLT according to the time of fat load ingestion: 0700 h (diurnal (D) test) or 2200 h (nocturnal (N) test) in nine normal-weight healthy males. Baseline leptin concentration was correlated with the body mass index, body fat mass and percentage of body fat mass in both experiments. The leptin concentrations were higher in women than in men P , 0X001X In experiment 1, the leptin concentrations were higher in obese subjects than in controls, but did not change over time in either group. The plasma insulin concentrations at baseline and during the postprandial state, as well as the area under the curve (AUC) of insulin, were higher in obese subjects than in controls P , 0X05 2 0X0001X There was no correlation between postprandial insulin responses and postprandial leptin responses in either obese or control groups. In experiment 2, leptin (D vs N, 2X9^1X4 vs 2X9^1X0 ngaml) and insulin (D vs N, 41^18 vs 25^9 pmolal) concentrations were similar at the beginning of the D and N tests after a 10 h fast. The leptin concentrations did not change after D or N tests and were not statistically different for D and N tests. Our results indicate that the leptin concentration in healthy controls and in obese patients is not acutely influenced by a high fat load.

Effect of high-fat meals and fatty acid saturation on postprandial levels of the hormones ghrelin and leptin in healthy men

“…Cross-sectional studies show an association between fasting leptin and insulin (Rosenbaum et al, 1997), as do long-term (Kolaczynski et al, 1996b;Boden et al, 1997) but not short-term (Dagogo-Jack et al, 1996) insulin infusion and some postprandial studies (Romon et al, 1999;Koutsari et al, 2003). Our data were in line with a number of studies which fail to show significant correlation between leptin and insulin after consumption of HF, mixed and even high-CHO meals (Sinha et al, 1996;Pratley et al, 1997;Guerci et al, 2000;Herrmann et al, 2001;Poretsky et al, 2001). If insulin is a driving force in the control of leptin release (Havel et al, 1999;Romon et al, 1999Romon et al, , 2003Evans et al, 2001;Koutsari et al, 2003;Fogteloo et al, 2004), it is possible that this mechanism is important only when a major portion of the diet comprises CHO.…”

“…Not all HF trials however show a decrease in serum leptin. Hormone levels were unchanged in lean and obese subjects given HF meals both morning and evening (Guerci et al, 2000), in lean (Monteleone et al, 2003) and obese subjects (Weigle et al, 1997) who responded to neither HF or high-CHO, and those who responded to high-CHO but not to HF (Tentolouris et al, 2003). Numerous studies investigating long-term effects of HF feeding have failed to show a response of fasting leptin to diet (Havel et al, 1996;Schrauwen et al, 1997;Weigle et al, 1997) but the collection of only a morning fasted sample for hormone analysis may make the interpretation of these studies difficult.…”

“…There is little or no correlation between the two hormones in several postprandial studies (Dagogo-Jack et al, 1996;Sinha et al, 1996;Pratley et al, 1997;Guerci et al, 2000;Herrmann et al, 2001;Poretsky et al, 2001) and this has lead to a revived interest in the influence of other dietary nutrients, including lipids, which have a blunted effect on insulin compared to CHO. Other trials which have shown a decrease in leptin after a fatty meal include lean (Romon et al, 1999) and obese subjects (Imbeault et al, 2001), and where HF test meals have followed high-and low-CHO acclimation (Koutsari et al, 2003).…”

“…Whether high-fat (HF) diets associated with obesity may modulate leptin is less clear, failing to alter fasting leptin during energy balance (Schrauwen et al, 1997) and weight stability (Weigle et al, 1997), or during overfeeding (Dirlewanger et al, 2000). The postprandial response to HF feeding set against a diurnal change in circulating leptin is even more variable and circulating levels may increase (Dallongeville et al, 1998;Imbeault et al, 2001), decrease (Havel et al, 1999;Romon et al, 1999;Evans et al, 2001;Imbeault et al, 2001;Koutsari et al, 2003), or not change (Weigle et al, 1997;Guerci et al, 2000;Monteleone et al, 2003;Tentolouris et al, 2003) following a fatty meal. Changes in both hormones in response to dietary fat are commonly less pronounced than for CHO (Havel et al, 1999;Romon et al, 1999;Monteleone et al, 2003;Greenman et al, 2004) and it has been suggested that insulin may play a critical role in regulation (Evans et al, 2001;Mohlig et al, 2002;Saad et al, 2002;Flanagan et al, 2003;Koutsari et al, 2003;Fogteloo et al, 2004).…”

Leptin secretion after a high-fat meal in normal-weight rats: strong predictor of long-term body fat accrual on a high-fat diet

“…In normal-weight animals, an HFM compared with premeal scores produces increases in insulin, leptin, glucose, and lipids, but causes little change in CORT (22,59). Most interesting is the finding in clinical studies that this HFM-induced increase in insulin and lipids is significantly greater in the obese compared with lean subjects (21,24). Thus the acute response after a meal may very likely contribute to the chronic endocrine and metabolic disturbances typically seen in obese subjects.…”