Beneficial effects of ketogenic diet in obese diabetic subjects

Dashti, H.; Mathew, T.C.; Khadada, Mousa; Al-Mousawi, Æ Mahdi; Talib, Husain; Asfar, Sami; Behbahani, Abdulla I.; Al-Zaid, N. S.

doi:10.1007/s11010-007-9448-z

Cited by 152 publications

(174 citation statements)

References 41 publications

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“…␤-Cell area and pancreas area were determined using an image analysis program (Stacks 2.1; LUMC), excluding large blood vessels, larger ducts, adipose tissue, and lymph nodes as previously described (11). ␤-Cell mass was determined by the ratio of ␤-cell area to pancreas area multiplied by the pancreas weight.…”

Section: Animalsmentioning

confidence: 99%

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Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice

Ellenbroek

Dijck

Töns

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

123

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Ellenbroek JH, van Dijck L, Töns HA, Rabelink TJ, Carlotti F, Ballieux BE, de Koning EJ. Long-term ketogenic diet causes glucose intolerance and reduced ␤-and ␣-cell mass but no weight loss in mice. Am J Physiol Endocrinol Metab 306: E552-E558, 2014. First published January 7, 2014 doi:10.1152/ajpendo.00453.2013.-High-fat, low-carbohydrate ketogenic diets (KD) are used for weight loss and for treatment of refractory epilepsy. Recently, short-time studies in rodents have shown that, besides their beneficial effect on body weight, KD lead to glucose intolerance and insulin resistance. However, the long-term effects on pancreatic endocrine cells are unknown. In this study we investigate the effects of long-term KD on glucose tolerance and ␤-and ␣-cell mass in mice. Despite an initial weight loss, KD did not result in weight loss after 22 wk. Plasma markers associated with dyslipidemia and inflammation (cholesterol, triglycerides, leptin, monocyte chemotactic protein-1, IL-1␤, and IL-6) were increased, and KD-fed mice showed signs of hepatic steatosis after 22 wk of diet. Long-term KD resulted in glucose intolerance that was associated with insufficient insulin secretion from ␤-cells. After 22 wk, insulin-stimulated glucose uptake was reduced. A reduction in ␤-cell mass was observed in KD-fed mice together with an increased number of smaller islets. Also ␣-cell mass was markedly decreased, resulting in a lower ␣-to ␤-cell ratio. Our data show that long-term KD causes dyslipidemia, a proinflammatory state, signs of hepatic steatosis, glucose intolerance, and a reduction in ␤-and ␣-cell mass, but no weight loss. This indicates that long-term high-fat, lowcarbohydrate KD lead to features that are also associated with the metabolic syndrome and an increased risk for type 2 diabetes in humans. pancreatic islet; ketogenic diet; glucose intolerance; ␤-cell; ␣-cell

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Section: Animalsmentioning

confidence: 99%

“…HIGH-FAT, LOW-CARBOHYDRATE KETOGENIC DIETS (KD) are used in weight loss programs and are associated with improvement of the glycemic status in obese subjects (30,35) and patients with type 2 diabetes (11,19). KD are also used as an effective treatment for refractory epilepsy (7,27,33).…”

mentioning

confidence: 99%

Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice

Ellenbroek

Dijck

Töns

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

123

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“…Long-term periods of KD maintenance led to decreased plasma triglyceride levels in diabetic patients (Yancy et al, 2005;Dashti et al, 2007). Therefore, we investigated the effect of KD on plasma triglyceride concentrations in chicken.…”

Section: Discussionmentioning

confidence: 99%

“…KD also induces weight loss or slower weight gain in mammals, despite having high lipid content (Dashti et al, 2007;Kennedy et al, 2007). In addition, since ketone bodies are mediators of fatty acid β-oxidation in the liver, the effect of KD or ketosis on plasma lipid levels and lipid metabolism has been investigated in mammals.…”

Section: Introductionmentioning

confidence: 99%

Plasma Lipid Profiles and Redox Status are Modulated in a Ketogenic Diet-Induced Chicken Model of Ketosis

et al. 2013

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Ketone bodies such as β-hydroxybutyrate and acetoacetate have physiological functions in addition to being used as an energy source. In order to assess the effect of elevated ketogenesis on blood lipid profiles and redox status, a ketogenic diet (KD), a high-fat, low-carbohydrate, and low-protein diet, was fed to chicken for 4 weeks. Plasma β-hydroxybutyrate, but not acetoacetate, concentrations were significantly increased by KD feeding for 2 and 4 weeks. The KD also induced elevation of plasma non-esterified fatty acid (NEFA) and total cholesterol concentrations, whereas plasma triglyceride concentration was decreased. Plasma total antioxidant activity in chicken with ketosis induced by KD was lower than that of the control. However, the level of plasma TBARs, an oxidative stress marker, was also reduced by KD feeding. A reduction of energy intake was observed in chickens fed the KD; therefore, the effect of a restricted diet (RD) was also investigated. Plasma β-hydroxybutyrate concentration, lipid (total cholesterol and NEFA) concentration, and redox status were not affected by RD feeding. These data suggest that a high-fat, lowcarbohydrate, and low-protein diet induces ketosis by elevating blood β-hydroxybutyrate concentration in chicken. Under conditions of ketosis induced by the KD, total antioxidant capacity was reduced along with a modulation of the blood lipid profile in chicken.

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“…As we will discuss below, reduction of glucose metabolism is likely more important for diabetic complications than reduction of blood glucose concentrations. A study of some interest used a similar design, in which patients with Type 2 diabetes were counseled to follow an Atkins-type diet over a period of a year [22]. Unfortunately ketones were not measured, but weight loss was substantial at the end of the year and of particular interest blood glucose was normalized after a year in diabetic patients with no effect of blood glucose in nondiabetic patients.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms by Which the Ketogenic Diet Reverses Obesity and Diabetes

Moreno¹

2017

EMIJ

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Since the beginning of the 20th century, when low-carbohydrate diets were first implemented to treat Type 1 diabetes, the role of dietary composition in regulating glucose homeostasis and, increasingly, energy balance, has been the subject of great interest to both biomedical researchers and, increasingly, to the public. In fairly extreme circumstances (e.g., Type 1 diabetes untreated with insulin) low-carbohydrate diets (which are generally high-fat diets) can be useful to reduce blood glucose, but since the advent of insulin therapy, and increasing appreciation of the cardiovascular consequences of hyperlipidemia, clinical practice has dramatically favored highcarbohydrate, low-fat diets for diabetes (especially Type 2 diabetes, largely associated with obesity). This clinical advice, at the time, seemed fairly radical. In a famous treatise, "The Physiology of Taste" published in 1825, Brillat-Savarin, argue that consumption of "natural" diets (e.g., meat and vegetables) promote health, whereas "cultivated" diet (e.g., derived from rice and wheat) increasingly led to deterioration of health associated with affluence.Similarly, in 1837 Sylvester Graham published "A treatise on bread and breadmaking", essentially a tirade against food with grains (as well as meat), which were not suited to the assumption that gluttony was among the greatest sins (clearly a theme in subsequent American diet fads). Similarly throughout the 20th century popular diets (including those promotes by Adelle Davis in the 1950s, Robert Atkins in the 1970s, the paleo diet, and increasingly many more) have emphasized lowcarbohydrate, high-fat diets especially for weight loss (viewed by the public as a more compelling concern than glucose homeostasis). While these diets have little if any clinical evidence for efficacy, low-calorie, low-protein diets that produce ketogenesis are extremely effective to reverse obesity, hyperglycemia, and diabetic complications. The mini-review examines possible mechanisms mediating these remarkable effects, particularly focusing on epigenetic effects on hypothalamic neurons.

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Beneficial effects of ketogenic diet in obese diabetic subjects

Abstract: This study shows the beneficial effects of ketogenic diet in obese diabetic subjects following its long-term administration. Furthermore, it demonstrates that in addition to its therapeutic value, low carbohydrate diet is safe to use for a longer period of time in obese diabetic subjects.

Cited by 152 publications

References 41 publications

Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice

Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice

Plasma Lipid Profiles and Redox Status are Modulated in a Ketogenic Diet-Induced Chicken Model of Ketosis

Mechanisms by Which the Ketogenic Diet Reverses Obesity and Diabetes

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