A high-monounsaturated-fat/low-carbohydrate diet improves peripheral insulin sensitivity in non-insulin-dependent diabetic patients

Parillo, M.; Rivellese, Angela Albarosa; Ciardullo, Anna V.; Capaldo, Brunella; Giacco, Antonia; Genovese, Salvatore; Riccardi, Gabriele

doi:10.1016/0026-0495(92)90111-m

Cited by 190 publications

(113 citation statements)

References 30 publications

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“…The reduction in 2hPCG and trend toward increased muscle insulin sensitivity index on Low-CHO at 3 months is consistent with short-term studies suggesting that Low-CHO diets improve insulin sensitivity in type 2 diabetes [7,8]. Since exchanging saturated fat for MUFA does not improve insulin sensitivity if total fat intake is >37% energy [38], the short-term effect of low-carbohydrate/high-MUFA diets on insulin sensitivity may be due to reduced glucose toxicity resulting from lower postprandial glucose.…”

Section: Discussionsupporting

confidence: 80%

“…Ideally, dietary treatment would increase disposition index, either by improving insulin sensitivity or insulin secretion or both. Low-carbohydrate, high-monounsaturated-fattyacids (MUFA) [7,8], or low-glycaemic-index diets [9], may improve insulin sensitivity in individuals with type 2 diabetes, but little is known about the effects of such diets on beta cell function in type 2 diabetes. Furthermore, the studies cited were of short duration (2-5 weeks) and it is not known whether the short-term effects persist over a longer period of time.…”

Section: Introductionmentioning

confidence: 99%

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Low glycaemic index diet and disposition index in type 2 diabetes (the Canadian trial of Carbohydrates in Diabetes): a randomised controlled trial

Wolever

Mehling²,

Chiasson

et al. 2008

Diabetologia

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Aims/hypothesis We recently found that oral glucose tolerance over 1 year in type 2 diabetic patients declined to a significantly lesser degree on a low-glycaemic-index than on a reduced-carbohydrate diet. Here, we examined whether that finding was associated with an improvement in disposition index, an index of beta cell function defined as the product of insulin sensitivity and insulin secretion. Since this is a report of secondary analysis on a previously published trial, the results should be considered as hypothesis-generating. Methods Type 2 diabetic patients treated by diet alone (n=162) were randomised by computer to high-carbohydrate/highglycaemic index (High-GI, n=52), high-carbohydrate/lowglycaemic index (Low-GI, n=56) or low-carbohydrate/ high-monounsaturated-fat (Low-CHO, n= 54) diets for 1 year in a multi-centre, parallel-design clinical trial conducted at University teaching hospitals. At baseline and at 3, 6 and 12 months participants underwent 75 g OGTTs; 27 participants dropped out or were excluded. Indices of insulin sensitivity, insulin secretion and disposition index, derived from the OGTT, were compared among diets. Those assessing the outcomes were blinded to group assignment. Results Neither muscle insulin sensitivity index nor insulinogenic index differed significantly among diets. However, a significant time×diet interaction existed for disposition index (muscle insulin sensitivity index×insulinogenic index) (p=0.036). After 3 months, disposition index tended to be higher on Low-CHO than on Low-GI diets, namely by 0.07 h −1 (95% CI −0.04, 0.18). However, by 12 months this reversed and disposition index became higher on Low-GI than on Low-CHO, namely by 0.12 h −1 (0.01, 0.23; p< 0.05, baseline disposition index 0.23 h −1 ). There were no important adverse effects associated with the treatments. Conclusions/interpretation These results suggest that, in patients with type 2 diabetes on diet alone, a Low-GI diet for 1 year increases disposition index, an index of beta cell function, compared with a Low-CHO diet.

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Low glycaemic index diet and disposition index in type 2 diabetes (the Canadian trial of Carbohydrates in Diabetes): a randomised controlled trial

Wolever

Mehling²,

Chiasson

et al. 2008

Diabetologia

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“…For example, conventional dietary recommendations for gout have focused on restriction of purine intake, although low-purine diets are often high in carbohydrate and saturated fat (7). These macronutrients are associated with an increased risk of insulin resistance syndrome and associated major consequences (21,32,33). Furthermore, these macronutrients tend to lead to higher serum insulin levels, which are known to reduce renal excretion of urate (11,19 -21), thus potentially raising the serum uric acid level and the risk of gout.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of the metabolic syndrome in patients with gout: The Third National Health and Nutrition Examination Survey

Choi¹,

Ford²,

Li³

et al. 2007

Arthritis & Rheumatism

411

216

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Objective. To determine the prevalence of metabolic syndrome among patients with gout and to examine the association between the 2 conditions in a nationally representative sample of US adults. Methods. Using data from 8,807 participants age >20 years in the Third National Health and Nutrition Examination Survey (1988 -1994), we determined the prevalence of metabolic syndrome among individuals with gout and quantified the magnitude of association between the 2 conditions. We used both the revised and original National -4.61), respectively. With the original NCEP/ATP criteria, the corresponding prevalences were slightly lower, whereas the corresponding odds ratios were slightly higher. The stratified prevalences of metabolic syndrome by major associated factors of gout (i.e., body mass index, hypertension, and diabetes) remained substantially and significantly higher among those with gout than those without gout (all P values <0.05). Conclusion. These findings indicate that the prevalence of metabolic syndrome is remarkably high among individuals with gout. Given the serious complications associated with metabolic syndrome, this frequent comorbidity should be recognized and taken into account in long-term treatment and overall health of individuals with gout.

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“…The studies that have been carried out generally find that high-fat feeding causes an impairment of glucose tolerance [1,2,3], but in one study where insulin sensitivity was carefully measured by clamping studies it was found that insulin sensitivity actually increased [36].…”

Section: Discussionmentioning

confidence: 99%

Saturated-fat diet induces moderate diabetes and severe glomerulosclerosis in hamsters

Popov¹,

Simionescu²,

Shepherd

2003

Diabetologia

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Aims/hypothesis. Diets high in saturated fat are thought to be a risk factor for Type 2 diabetes and associated complications. We investigated effects of a medium and high saturated fat diet on the development of diabetes-associated pathologies in Golden Syrian hamsters, an animal that reacts to dietary lipids in a fashion similar to humans. Methods. Three diets containing 46.5 kcal %, 267.3 kcal %, and 488.2 kcal % as saturated fat respectively, were studied. Metabolic parameters were measured up to 20 weeks. Electron microscopy was used to examine the structure of the pancreas, aorta and kidney. Results. Increased saturated fat consumption was associated with: (i) gradual imbalance of homeostasis, and severe structural alterations of acinar, beta cells and capillaries in the pancreas, and of the kidney glomeruli; (ii) severe hypertriglyceridaemia and augmented creatinine concentrations related to disturbances of the renal function, progressing to nodular glomerulosclerosis and nephropathy; (iii) reduced early insulin secretion in response to glucose; (iv) switch of the aortic endothelium to a secretory phenotype. Conclusion/interpretation. The results show that highcaloric saturated fat intake induced diabetes in hamsters, probably linked to delayed insulin secretion. The model was also associated with the development of a range of pathologies characteristic to human diabetes, including nephropathy and defects in vasculature. Thus, high-fat fed hamsters provide a new model that is likely to be useful in understanding the cellular and molecular mechanisms involved in the pathogenesis of diabetes. [Diabetologia (2003[Diabetologia ( ) 46:1408[Diabetologia ( -1418

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A high-monounsaturated-fat/low-carbohydrate diet improves peripheral insulin sensitivity in non-insulin-dependent diabetic patients

Cited by 190 publications

References 30 publications

Low glycaemic index diet and disposition index in type 2 diabetes (the Canadian trial of Carbohydrates in Diabetes): a randomised controlled trial

Low glycaemic index diet and disposition index in type 2 diabetes (the Canadian trial of Carbohydrates in Diabetes): a randomised controlled trial

Prevalence of the metabolic syndrome in patients with gout: The Third National Health and Nutrition Examination Survey

Saturated-fat diet induces moderate diabetes and severe glomerulosclerosis in hamsters

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