Short-Term Physiological Effects of a Very Low-Calorie Ketogenic Diet: Effects on Adiponectin Levels and Inflammatory States

Huang

Chem. Biol. Technol. Agric.

et al. 2020

Background The ketogenic diet (KD) can promote the anti-inflammatory metabolic state and increase ketone body level in rats. This study was to explore the effects and differences of KD with or without medium-chain fatty acids (MCFAs) on serum inflammatory factors and mTOR pathway in Sprague–Dawley (SD) rats. Results Male SD rats were assigned to five groups: control diet (C), 20% caloric restriction diet (LC), 20% caloric restriction ketogenic diet (containing MCFAs) (LCKD1), 20% caloric restriction ketogenic diet (LCKD2) and 20% caloric restriction foreign ketogenic diet (LCKD3), and fed for 30 d. LC and KD could significantly reduce the body weight of rats; LC and KD containing MCFAs showed anti-inflammatory effects; KD without MCFAs decreased the concentration of mTOR1, while KD containing MCFAs decreased the expression of AMPK, mtor1 and P70sk. Conclusions KD containing MCFAs showed better effects on the mTOR pathway and anti-inflammation than that without MCFAs.

Section: Discussionsupporting

confidence: 93%

Effects of ketogenic diet containing medium-chain fatty acids on serum inflammatory factor and mTOR signaling pathway in rats

Huang

Chem. Biol. Technol. Agric.

et al. 2020

“…The effect was a significant decrease in body weight, body mass index, waist circumference, hip circumference, body fat %, and decreased fasting leptin levels. Similar positive outcomes were seen in other KD diet studies [ 56 , 63 , 64 ]. Similarly, a recent meta-analysis concluded that very low-calorie ketogenic diets are a very effective strategy for treating obesity [ 65 ].…”

Section: The Effect Of the Ketogenic Diet On Weight Losssupporting

confidence: 88%

The Potential Health Benefits of the Ketogenic Diet: A Narrative Review

2021

Considering the lack of a comprehensive, multi-faceted overview of the ketogenic diet (KD) in relation to health issues, we compiled the evidence related to the use of the ketogenic diet in relation to its impact on the microbiome, the epigenome, diabetes, weight loss, cardiovascular health, and cancer. The KD diet could potentially increase genetic diversity of the microbiome and increase the ratio of Bacteroidetes to Firmicutes. The epigenome might be positively affected by the KD since it creates a signaling molecule known as β-hydroxybutyrate (BHB). KD has helped patients with diabetes reduce their HbA1c and reduce the need for insulin. There is evidence to suggest that a KD can help with weight loss, visceral adiposity, and appetite control. The evidence also suggests that eating a high-fat diet improves lipid profiles by lowering low-density lipoprotein (LDL), increasing high-density lipoprotein (HDL), and lowering triglycerides (TG). Due to the Warburg effect, the KD is used as an adjuvant treatment to starve cancer cells, making them more vulnerable to chemotherapy and radiation. The potential positive impacts of a KD on each of these areas warrant further analysis, improved studies, and well-designed randomized controlled trials to further illuminate the therapeutic possibilities provided by this dietary intervention.

“…Most adiponectin presents in the serum as an oligomer, including low molecular weight (LMW), medium molecular weight (MMW), and high molecular weight (HMW). 3 Among them, HMW is considered as the most biologically active. Serum adiponectin concentration ranges widely in healthy adults.…”

Section: Discussionmentioning

confidence: 99%

“…Monda et al found that adiponectin concentration mean in people with obesity was 10.8 μg/mL with a standard deviation of 1.2 (10.8±1.2), which could be increased to 25.55±1.3 μg/mL by a very low-calorie ketogenic diet. 3 From the above evidences, it is suggested that the functions of adiponectin are closely associated with its concentrations. Moreover, Negoro et al found that low adiponectin concentration is responsible for the systemic inflammation in adiponectin anti-sense transgenic mice.…”

Section: Discussionmentioning

confidence: 99%

“…Adiponectin is well known as a beneficial adipokine that could increase insulin sensitization and display anti-inflammatory, anti-atherogenic, and anti-diabetic effects. [1][2][3] The metabolism effects may involve in the activation of the cell surface receptors, AdipoR1 and AdipoR2, to enhance oxidation of fatty acid and uptake of glucose in muscle and decrease gluconeogenesis in the liver. [4][5][6] Adiponectin's antiatherogenic effects are associated with its anti-inflammation.…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms of Adiponectin in Regulation of Proinflammatory Cytokine Production and Migration in Macrophages

Jin¹,

Wang²

2021

JIR

Introduction Evidence indicate that adiponectin may exert pro-inflammatory effects on inflammatory cells. We have found that adiponectin knockout decreased inflammatory reaction and tubular damage in the ischemia-reperfusion kidney in APN-knockout mice. Globular adiponectin and full-length adiponectin (g-APN and f-APN) were used in this study to investigate the effects of adiponectin on proinflammatory cytokines production and migration in Raw 264.7 cells. Methods Proinflammatory cytokines production was detected by real-time RT-PCR. NF-kappaB activation was interrupted through Ad-DN-IκBα or SN-50 to confirm how g-APN induces proinflammatory cytokines production. The siRNA against AdipoR1 and AdipoR2 was investigated to uncover the signaling pathway that may involve in NF-kappaB activation and migration in Raw 264.7 cells. Results g-APN, not f-APN, was found triggering the production of inflammatory cytokine MIP-2, IL-6, TNFα, and MCP-1 in Raw 264.7 cells. NF-kappaB Inhibition by Ad-DN-IκBα expression or cell-permeable NF-κB inhibitor SN-50 could decrease NF-kappaB nuclear translocation and subsequently decrease inflammatory cytokine expression triggered by globular ANP. However, AdipoR1 and AdipoR2 were not found involved in NF-kappaB activation in this study. Full-length APN, not g-APN, was involved in the promotion of macrophage migration. The migration induced by full-length APN could be inhibited by knockdown of AdipoR1 expression with siRNA. The migration effect could also be inhibited by PI 3 Kγ inhibitor, AS-605240. Discussion These results suggested that full-length adiponectin increases macrophage migration through Adiponectin-AdipoR1-PI 3 Kgamma signaling pathway. However, NF-κB activation induced by g-APN in this study was independent of AdipoR1 or AdipoR2. The exact signaling pathway of NF-κB activation by adiponectin should be further studied to find a new anti-inflammatory target.