A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice

Lamont, Benjamin J.; Waters, Matthew F.; Andrikopoulos, Sofianos

doi:10.1038/nutd.2016.2

Cited by 52 publications

(54 citation statements)

References 55 publications

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“…For example, one study stated that "Long-term highfat, low-carbohydrate KD leads to features that are also associated with the metabolic syndrome and an increased risk for type 2 diabetes in humans" [1]. Two other studies reported that "Use of LC-HF diets … should be balanced against potentially harmful metabolic side effects" [2] and that "Our results do not support the recommendation of an LCHFD for use in prediabetes [3]. Moreover, based on that last study, the news media reported to the public that "Following a low-carbohydrate, high-fat diet for just eight weeks can lead to rapid weight gain and health complications, a new mouse study has demonstrated.…”

Section: Introductionmentioning

confidence: 64%

“…It was found that, despite preventing weight gain in mice, the KD induces insulin resistance [37]. In addition, it was later shown that the KD causes glucose intolerance without weight loss in mice [1], and even increases weight gain and glucose intolerance in New Zealand Obese mice [3]. Other studies also reported insulin resistance and glucose intolerance in rodents fed a KD [1,2,[38][39][40][41][42].…”

Section: Self-contradictory Results In Rodentsmentioning

confidence: 99%

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The mystery of the ketogenic diet: benevolent pseudo-diabetes

Blagosklonny

2019

Cell Cycle

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Designed a century ago to treat epilepsy, the ketogenic diet (KD) is also effective against obesity and diabetes. Paradoxically, some studies in rodents have found that the KD seemingly causes diabetes, contradicting solid clinical data in humans. This paradox can be resolved by applying the concept of starvation pseudo-diabetes, which was discovered in starved animals almost two centuries ago, and has also been observed in some rapamycin-treated rodents. Intriguingly, use of the KD and rapamycin is indicated for a similar spectrum of diseases, including Alzheimer’s disease and cancer. Even more intriguingly, benevolent (starvation) pseudo-diabetes may counteract type 2 diabetes or its complications.

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Section: Introductionmentioning

confidence: 64%

Section: Self-contradictory Results In Rodentsmentioning

confidence: 99%

The mystery of the ketogenic diet: benevolent pseudo-diabetes

Blagosklonny

2019

Cell Cycle

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“…It should be noted that there are some papers that correlate increased risk of developing glucose intolerance and noninsulin-dependent diabetes mellitus with the LCHF diet [42]. On the other hand, in mice it is already shown in the literature that the LCHF diet is found to increase weight gain and does not improve the glycemic profile [43]. These differences might correlate with the differences of metabolism present in different species.…”

Section: Discussionmentioning

confidence: 99%

Metformin Reduces Lipogenesis Markers in Obese Mice Fed a Low‐Carbohydrate and High‐Fat Diet

Santana

Lelis

Mendes

et al. 2016

Lipids

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Lipogenesis is the process by which fatty acids are synthesized. In metabolic syndrome, an insulin resistant state along with high plasma levels of free fatty acids (FFA) and hyperglycemia may contribute to the lipogenic process. The aim of the present study was to investigate the effects of oral administration of metformin on the expression of lipogenic genes and glycemic profile in mice fed with low-carbohydrate high-fat diet by evaluating their metabolic profile. SWISS male mice were divided into 4 groups (N = 7) that were fed with standard (ST), standard plus metformin (ST + MET), low-carbohydrate high-fat diet (LCHFD) and low-carbohydrate high-fat diet plus metformin (LCHFD + MET) (100 mg kg diet) diets respectively. Food intake, body weight and blood parameters, such as glucose tolerance, insulin sensitivity, glucose, HDL-c, total cholesterol, triglycerides, ASL and ALT levels were assessed. Histological analyses were performed on hematoxylin and eosin-stained epididymal adipose tissue histological specimens. The expression levels of peroxisome proliferator-activated receptor (PPARγ), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), were assessed by RT-PCR. This study showed that metformin decreased adipocyte area, body weight and food consumption in obese animals when compared to the standard group. Furthermore, the expression of lipogenic markers in adipose tissue were diminished in obese animals treated with metformin. This data showed that oral administration of metformin improved glucose and lipid metabolic parameters in white adipose tissue by reducing the expression of lipogenesis markers, suggesting an important clinical application of MET in treating obesity-related diseases in metabolic syndrome.

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“…Low-carbohydrate, high-protein, low-energy diets are widely used in weight management programs. A growing body of evidence suggests that the high-protein, low-carbohydrate diets improve hyperinsulinemia [44]. These results suggest a similar control mechanism of metabolic stores and insulin signaling in both vertebrates and suggest that developmental diets can influence the insulin-signaling mediated life-history traits during adult life, and these affects vary in males and females, suggesting sex-specific differences in nutrient regulation.…”

Section: Discussionmentioning

confidence: 87%

Nutritional Quality during Development Alters Insulin-Like Peptides Expression and Physiology of the Adult Yellow Fever Mosquito, <em>Aedes aegypti</em>

Pooriirouby¹,

Sharma²,

Beard³

et al. 2018

Preprint

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Abstract:Mosquitoes have distinct developmental and adult life history, and the vectorial capacity of females has been shown to be affected by the larval nutritional environment. However, little is known about the effect of developmental nutrition on insulin-signaling and nutrients storage. In this study, we used Aedes aegypti, the yellow fever mosquito, to determine whether larval nutrition affects insulin gene expression. We also determined the traits regulated by insulin signaling, such as stored-nutrients levels and fecundity. We raised mosquito larvae on two different diets, containing either high protein or high carbohydrates. Development on a highcarbohydrate diet resulted in several life-history phenotypes indicative of suboptimal conditions, including increased developmental time and decreased fecundity. Additionally, our data showed that insulin transcript levels are affected by a high-carbohydrate diet during development.Females, not males, reared on high-carbohydrate diets had much higher transcript levels of insulin-like peptide 3 (ILP3), a mosquito equivalent of human insulin, and these females more readily stored sugar from the meal into lipids. We also found that AaILP4, not AaILP3, transcript levels were much higher in the males after a sugar meal, suggesting sex-specific differences in insulin-signaling pathway. Our findings suggest a conserved mechanism of carbohydratemediated hyperinsulinemia in animals.

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A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice

Cited by 52 publications

References 55 publications

The mystery of the ketogenic diet: benevolent pseudo-diabetes

The mystery of the ketogenic diet: benevolent pseudo-diabetes

Metformin Reduces Lipogenesis Markers in Obese Mice Fed a Low‐Carbohydrate and High‐Fat Diet

Nutritional Quality during Development Alters Insulin-Like Peptides Expression and Physiology of the Adult Yellow Fever Mosquito, <em>Aedes aegypti</em>

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