Dietary Modulation of Circulating Leptin Levels: Site-Specific Changes in Fat Deposition and Ob mRNA Expression

Walker, Celia G.; Bryson, Janet M.; Phuyal, Jenny L.; Caterson, Ian D.

doi:10.1055/s-2002-26707

Cited by 17 publications

(26 citation statements)

References 33 publications

(48 reference statements)

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“…30,31 The amount of leptin mRNA was reduced in fasted rats prior to the glucose challenge, as previously reported. 4,5,30,32 This decreased amount of leptin mRNA in EWAT of fasted rats may reduce the capacity for de novo leptin synthesis compared to the EWAT of fed rats.…”

Section: Discussionsupporting

confidence: 76%

Insulin determines leptin responses during a glucose challenge in fed and fasted rats

et al. 2005

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OBJECTIVE: Leptin secretion has been shown to respond acutely to changes in blood glucose and insulin. Nutritional state also has a marked effect on both the level of circulating leptin protein and leptin gene expression. The aim of this study was to assess whether the prior nutritional state altered the leptin secretory response to an acute glucose challenge, and to determine potential mechanisms. DESIGN: Male fed or fasted rats (200-250 g) were administered a single intravenous glucose bolus (1, 4 or 7 g/kg). The serum leptin, glucose, insulin and free fatty acid responses were studied over the following 5 h. The level of leptin gene expression and leptin protein was then determined in the epididymal fat pads, and in fed and fasted untreated rats for basal comparison. RESULTS: Leptin secretion in response to glucose was suppressed in fasted rats following all glucose doses. The total leptin response was correlated with the total insulin response in all conditions (r ¼ 0.85) and with the glucose response in fed rats (r ¼ 0.69). Both leptin gene expression and leptin protein content were lower in basal fasted rats. Leptin gene expression and leptin protein content still remained lower 5 h following a glucose bolus but there was partial reversal of the effects of fasting following the 7 g/kg glucose dose. CONCLUSIONS: Leptin secretion in response to an intravenous glucose bolus was determined by the insulin response and was significantly suppressed in fasted compared to fed rats. In addition to differences in the total insulin response of the animals, lower leptin responses may be facilitated by lower levels of both leptin gene mRNA and pre-existing leptin protein in epididymal adipose tissue of fasted rats.

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Section: Discussionsupporting

confidence: 76%

Insulin determines leptin responses during a glucose challenge in fed and fasted rats

et al. 2005

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“…Animal studies show a more consistent effect of dietary GI on the leptin response and support the idea that dietary macronutrient content as well as dietary GI contribute to variations in circulating plasma leptin levels [39,40] . Animal studies uniformly observe that following a high glycemic diet both plasma leptin and leptin mRNA expression in fat are significantly decreased [39,40] .…”

Section: Discussionsupporting

confidence: 63%

“…Animal studies uniformly observe that following a high glycemic diet both plasma leptin and leptin mRNA expression in fat are significantly decreased [39,40] . Recently, Pawlak et al [41] demonstrated the independent and adverse effects of dietary glycemic index on body composition and risk factors for diabetes and cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

A High Glycemic Meal Suppresses the Postprandial Leptin Response in Normal Healthy Adults

Barkoukis

Marchetti²,

Nolan

et al. 2007

Ann Nutr Metab

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Background/Aims: To evaluate the metabolic effects of meals with varying glycemic index (GI). Methods: We measured the glucose, insulin and leptin responses to two contrasting breakfast cereals in a group of 10 young healthy volunteers. Meals were provided on two separate occasions in random order after a 12-hour overnight fast, and consisted of 50 g of available carbohydrate from either Corn Flakes (Kellogg’s), or Fiber One® (General Mills). Blood samples were obtained at rest, and 30, 60, 90 and 120 min after eating. The GI was calculated from the glucose response to the test meal normalized against a 50 g oral glucose load. Results: The GI for Corn Flakes was 125 ± 17 units and 49 ± 8 units for Fiber One®. These meals were classified as high GI and low GI, respectively, and were significantly different from each other (p < 0.0003). The area under the insulin response curve (AUC) following the low glycemic meal was significantly attenuated compared to the high glycemic meal (14,064 ± 2,694 vs. 6,828 ± 1,182 pmol/l·min, p < 0.02). The leptin AUC revealed that circulating leptin was suppressed by the high glycemic meal compared to the low (3.1 ± 1.5 vs. 9.6 ± 3.6 ng/ml·min, p < 0.04). Conclusions: Lower insulin and higher leptin suggests that low glycemic meals promote a postprandial metabolic milieu that is favorable for reduced food consumption; this may be advantageous in the control of obesity and related disorders including insulin resistance and type 2 diabetes.

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“…Effects of high-vs. low-GI diets on molecular markers of fat metabolism have been investigated only in a few previous studies (12,23,24). After long-term high-vs. low-GI exposure, the expression of important enzymes in regulation of de novo lipogenesis such as Acc and Fas was significantly elevated.…”

Section: Discussionmentioning

confidence: 99%

Impairment of fat oxidation under high- vs. low-glycemic index diet occurs before the development of an obese phenotype

Isken

Klaus²,

Petzke

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Exposure to high vs. low glycemic index (GI) diets increases fat mass and insulin resistance in obesity-prone C57BL/6J mice. However, the longer-term effects and potentially involved mechanisms are largely unknown. We exposed four groups of male C57BL/6J mice (n ϭ 10 per group) to long-term (20 wk) or short-term (6 wk) isoenergetic and macronutrient matched diets only differing in starch type and as such GI. Body composition, liver fat, molecular factors of lipid metabolism, and markers of insulin sensitivity and metabolic flexibility were investigated in all four groups of mice. Mice fed the high GI diet showed a rapid-onset (from week 5) marked increase in body fat mass and liver fat, a gene expression profile in liver consistent with elevated lipogenesis, and, after long-term exposure, significantly reduced glucose clearance following a glucose load. The long-term high-GI diet also led to a delayed switch to both carbohydrate and fat oxidation in the postprandial state, indicating reduced metabolic flexibility. In contrast, no difference in carbohydrate oxidation was observed after short-term high-vs. low-GI exposure. However, fatty acid oxidation was significantly blunted as early as 3 wk after beginning of the high-GI intervention, at a time where most measured phenotypic markers including body fat mass were comparable between groups. Thus long-term high-GI feeding resulted in an obese, insulin-resistant, and metabolically inflexible phenotype in obesity-prone C57BL/6J mice. Early onset and significantly impaired fatty acid oxidation preceded these changes, thereby indicating a potentially causal involvement. glycemic index; fat metabolism; body fat; insulin resistance; liver fat; metabolic flexibility; insulin resistance EXPOSURE TO HIGH VS. LOW glycemic index (GI) diets unfavorably affects fat mass and markers of insulin resistance in rodent models (1, 12, 15-17, 21, 23). Metabolic flexibility that can be defined as the capacity to adapt fuel oxidation to fuel availability (3, 7, 13) could also be changed by a high-GI diet, although no consensus exists as to whether diets varying in GI directly affect substrate oxidation or energy expenditure (4, 21). Alternatively, changes in substrate oxidation might be mainly a consequence of high-vs. low-GI diet-induced differences, e.g., in body weight, body fat distribution, or insulin resistance. Therefore, elucidating whether changes in substrate oxidation follow or precede an obese phenotype in high-GI-fed animals could be helpful for the understanding of potentially involved mechanisms.Most of the previous studies investigating effects of highvs. low-GI diets on metabolic markers were relatively short term (1,12,15,16,23), lasting between 3 and up to 13 wk. We are aware of only two previous longer-term studies, both of which reported unfavorable effects of high-vs. low-GI diets on body fat distribution and metabolic markers in rodents (17, 21). However, the first study (18 wk) investigated partial pancreatectomized male Sprague-Dawley rats, which is an animal mo...

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Dietary Modulation of Circulating Leptin Levels: Site-Specific Changes in Fat Deposition and Ob mRNA Expression

Cited by 17 publications

References 33 publications

Insulin determines leptin responses during a glucose challenge in fed and fasted rats

Insulin determines leptin responses during a glucose challenge in fed and fasted rats

A High Glycemic Meal Suppresses the Postprandial Leptin Response in Normal Healthy Adults

Impairment of fat oxidation under high- vs. low-glycemic index diet occurs before the development of an obese phenotype

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