Time course of insulin resistance associated with feeding dogs a high-fat diet

Rocchini, Albert P.; Marker, Paul H.; Cervenka, Tereza

doi:10.1152/ajpendo.1997.272.1.e147

Cited by 42 publications

(60 citation statements)

References 22 publications

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“…In fact, AIR G(0-19) showed a trend of increasing with fat feeding (P < 0.0005, linear trend). However, surprisingly, AIR G(0- 19) did not change at all in week 1 (P = NS, Table 5) and only began to increase by week 3 (P = NS), 2 weeks after the reduction in S I . The AIR G(0-19) peaked at week 6 (P < 0.0045) and then declined again toward the prediet value (P = 0.07, week 12 vs. week 0, not significant by Bonferroni correction).…”

Section: Resultsmentioning

confidence: 91%

“…Therefore, we report a model of central adiposity, limited weight gain, insulin resistance, but maintenance of normal glucose tolerance. Unlike models of fat overfeeding and massive weight gain (17)(18)(19)(20), the present model may be representative of modest weight gain in normal adults and therefore reveal the normal mechanisms by which homeostasis in response to central adiposity is maintained.…”

Section: Discussionmentioning

confidence: 99%

“…Insulin clearance was reduced in obesity (28)(29)(30)(31), insulin resistance without obesity (31), impaired glucose tolerance (IGT) (32), and diabetes (33). Decreased insulin clearance has also been observed with high-fat feeding in rats (34) and was suggested in a model of fat-fed dogs (19). Thus, the model of insulin resistance developed in this study is consistent with experimental and natural states of insulin resistance reported in the literature with respect to the compensation for insulin resistance.…”

Section: Longitudinal Compensation For Fat Feedingmentioning

confidence: 98%

“…Subsequently, insulin was injected (t = 20 min, 0.03 U/kg porcine insulin; Novo Nordisk, Copenhagen). We took 28 additional blood samples at t = 2, 3,4,5,6,8,10,12,14,16,19,22,23,24,25,30,40,50,60,70,80,90, 100, 110, 120, 140, 160, and 180 min for assay of glucose and insulin. Samples were taken into chilled tubes coated with lithium fluoride and heparin containing 50 µl EDTA, immediately centrifuged, and the plasma separated.…”

Section: Sd Mittelman and Associatesmentioning

confidence: 99%

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Longitudinal compensation for fat-induced insulin resistance includes reduced insulin clearance and enhanced beta-cell response.

et al. 2000

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Central adiposity is highly correlated with insulin resistance, which is an important risk factor for type 2 diabetes and other chronic diseases. However, in normal individuals, central adiposity can be tolerated for many years without development of impaired glucose tolerance or diabetes. Here we examine longitudinally the mechanisms by which glucose tolerance can be maintained in the face of substantial insulin resistance. Normal dogs were fed a diet enriched with moderate amounts of fat (2 g · kg -1 · day -1 ), similar to that seen in modern "cafeteria" diets, and the time course of metabolic changes in these animals was examined over 12 weeks. Trunk adiposity as assessed by magnetic resonance imaging increased from 12 to 19%, but body weight remained unchanged. Insulin sensitivity (S I ) as determined by frequently sampled intravenous glucose tolerance tests was measured over a 12-week period. S I decreased 35% by week 1 and remained impaired for the entire 12 weeks. Intravenous glucose tolerance was reduced transiently for 1 week, recovered to baseline, and then again began to decline after 8 weeks. Firstphase insulin response began to increase after week 2, peaked by week 6 (190% of basal), and then declined. The increase in insulin response was due partially to enhanced ␤-cell function (22%) but due also to añ 50% reduction in insulin clearance. This compensation by insulin clearance was also confirmed with insulin clamps performed in fat-fed versus control dogs. The present study confirms the ability of the normal individual to compensate for fat-induced insulin resistance by enhanced insulin response, such that the product of insulin sensitivity ؋ secretion is little changed. However, the compensation is due as much to reduced insulin clearance as increased ␤-cell sensitivity to glucose. Reduced hepatic extraction of insulin may be the first line of defense providing a higher proportion of secreted insulin to the periphery and sparing the ␤-cells during compensation for the insulin-resistant state. Diabetes 49:2116-2125, 2000 T here is abundant evidence that diabetes and obesity are increasing in the U.S. population (1-3). Because adiposity is related to insulin resistance (4-6), and insulin resistance is a risk factor for type 2 diabetes and cardiovascular disease, a consensus has emerged that increased adiposity is responsible for the increased incidence of type 2 diabetes and its associated morbidity (metabolic syndrome or syndrome X [7]). In addition, evidence has accumulated indicating that visceral adiposity in particular is associated with insulin resistance and the metabolic syndrome (8,9).Despite overwhelming evidence demonstrating association between insulin resistance, visceral adiposity, and metabolic risk, there is little evidence directly demonstrating that central adiposity in fact causes insulin resistance. In addition, there is little understanding of the mechanisms underlying the relationship among visceral adiposity, insulin resistance, and risk.To examine the acute effects of adiposi...

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Section: Resultsmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Longitudinal Compensation For Fat Feedingmentioning

confidence: 98%

Section: Sd Mittelman and Associatesmentioning

confidence: 99%

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Longitudinal compensation for fat-induced insulin resistance includes reduced insulin clearance and enhanced beta-cell response.

et al. 2000

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“…1,2 A high-fat diet can also induce hypertriglyceridemia, glucose intolerance and insulin resistance in animals. 3 The substitution of complex carbohydrate in the diet by simple sucrose has been shown to enhance plasma triacylglycerol (TAG) in animal studies. 4 Furthermore, feeding of a high-sucrose diet causes an increase in visceral fat accumulation in ventromedial hypothalamic (VMH)-lesioned obese and normal male Wistar rats.…”

Section: Introductionmentioning

confidence: 99%

Different origin of hypertriglyceridemia induced by a high-fat and a high-sucrose diet in ventromedial hypothalamic-lesioned obese and normal rats

Kageyama

Kashiba

et al. 2001

Int J Obes

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OBJECTIVE: To clarify the mechanism by which plasma triacylglycerol is affected by a high fat or a sucrose diet. DESIGN: Two sets of six groups each having six rats were prepared Ð (1) ventromedial hypothalamic (VMH)-lesioned rats fed a standard diet; (2) sham VMH-lesioned rats fed a standard diet; (3) VMH-lesioned rats fed a high-fat diet; (4) sham VMH-lesioned rats fed a high-fat diet; (5) VMH-lesioned rats fed a high-sucrose diet; and (6) sham VMH-lesioned rats fed a high-sucrose diet. After VMH lesions and sham operations, the rats were provided standard, high-fat and high sucrose diets for 2 weeks. Two weeks later, blood samples were collected after overnight fast to determine plasma triacylglycerol (TAG), hepatic triacylglycerol secretion rate (TGSR), fractional catabolic rate (FCR) of triacylglycerol and postheparin plasma lipoprotein lipase (LPL), plasma glucose, insulin and leptin. RESULTS: Values of TAG, TGSR, FCR and LPL in VMH-lesioned obese rats were all greater than those in sham-operated rats, regardless of the diet fed. In sham-operated rats, high-fat diet fed rats showed higher TAG with similar TGSR, higher LPL and lower FCR than those of standard diet fed rats. High-sucrose diet fed rats showed signi®cantly higher TAG with higher TGSR, higher LPL and lower FCR than those of standard diet fed rats. Moreover, high-sucrose diet fed rats showed higher TAG with higher TGSR, lower LPL and higher FCR than those of high-fat diet fed rats. In VMH-lesioned rats, high-fat diet fed rats showed higher TAG with similar TGSR, higher LPL and lower FCR than those of standard diet fed rats. High-sucrose diet fed rats showed markedly higher TAG with notably higher TGSR, higher LPL and lower FCR than those of standard diet fed rats. High-sucrose diet fed rats showed still higher TAG with markedly higher TGSR, similar LPL and higher FCR than those of high-fat diet fed rats. CONCLUSIONS: The mechanism by which TAG metabolism is affected by a high-fat or a high-sucrose diet differed; a high-fat diet increased plasma TAG level by lowering removal of TAG without increase in hepatic TAG secretion in sham-operated (normal) rats. A high-sucrose diet, in contrast, induced much higher plasma TAG levels by both increased hepatic TAG secretion and decreased removal of TAG. The effects of a high-fat or a high-sucrose diet were similar but exaggerated in VMH lesioned animals.

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Dietary-fat-induced obesity in mice results in beta cell hyperplasia but not increased insulin release: evidence for specificity of impaired beta cell adaptation

et al. 2005

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Time course of insulin resistance associated with feeding dogs a high-fat diet

Cited by 42 publications

References 22 publications

Longitudinal compensation for fat-induced insulin resistance includes reduced insulin clearance and enhanced beta-cell response.

Longitudinal compensation for fat-induced insulin resistance includes reduced insulin clearance and enhanced beta-cell response.

Different origin of hypertriglyceridemia induced by a high-fat and a high-sucrose diet in ventromedial hypothalamic-lesioned obese and normal rats

Dietary-fat-induced obesity in mice results in beta cell hyperplasia but not increased insulin release: evidence for specificity of impaired beta cell adaptation

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