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Sulforaphane improves leptin responsiveness in high-fat high-sucrose diet-fed obese mice.

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Diet-induced obesity (DIO) is commonly associated with hyperleptinemia and leptin resistance. Leptin acts centrally to inhibit food intake and increase energy expenditure, thereby preventing body weight gain. Resistance to the biological effects of leptin represents a major obstacle in utilizing

[Protective effects of sulforaphane on the oxidative damage of kidney mitochondria complex in obese rats induced by high-fat diet].

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OBJECTIVE To realize the oxidative damage of kidney mitochondrial complex in obese rats induced by high-fat diet and investigate the protective effects of sulforaphane against the damage. METHODS Eighty-eight adult male SD rats were used, after 1 week adaptability feeding, 8 rats were selected as

Sulforaphane Protects the Male Reproductive System of Mice from Obesity-Induced Damage: Involvement of Oxidative Stress and Autophagy.

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(1) Background: In recent decades, the prevalence of obesity has grown rapidly worldwide, thus causing many diseases, including male hypogonadism. Sulforaphane (SFN), an isothiocyanate compound, has been reported to protect the reproductive system. This research investigated the protective

Sulforaphane ameliorates glucose intolerance in obese mice via the upregulation of the insulin signaling pathway.

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Sulforaphane (SFN) is a dietary component with multiple bioactivities; however, its role in obesity-related metabolic derangement remains unclear. Here, the effect of SFN on the glucose intolerance of obese mice and the underlying mechanism were determined. C57B/6J male mice were randomly divided

Potential effects of sulforaphane to fight obesity.

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Obesity is linked to the onset of many diseases such as diabetes mellitus, cardiovascular diseases and cancer, among others. The prevalence of obesity nearly doubled worldwide between 1980 and 2014. Simultaneously, in the last decade, the effects of sulforaphane as a potential treatment for obesity

Sulforaphane suppresses obesity-related glomerulopathy-induced damage by enhancing autophagy via Nrf2

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Aims: Obesity-related glomerulopathy (ORG) is characterized by glomerulomegaly with or without focal and segmental glomerulosclerosis lesions. Isothiocyanate sulforaphane (SFN) can protect kidneys from ORG-related damages. In this study,

Sulforaphane improves dysregulated metabolic profile and inhibits leptin-induced VSMC proliferation: Implications toward suppression of neointima formation after arterial injury in western diet-fed obese mice.

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Sulforaphane (SFN), a dietary phase-2 enzyme inducer that mitigates cellular oxidative stress through nuclear factor erythroid 2-related factor 2 (Nrf2) activation, is known to exhibit beneficial effects in the vessel wall. For instance, it inhibits vascular smooth muscle cell (VSMC) proliferation,

Sulforaphane attenuates obesity by inhibiting adipogenesis and activating the AMPK pathway in obese mice.

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Obesity is associated with metabolic disorders. Sulforaphane, an isothiocyanate, inhibits adipogenesis and the occurrence of cardiovascular disease. In this study, we investigated whether sulforaphane could prevent high-fat diet (HFD)-induced obesity in C57BL/6N mice. Mice were fed a normal diet

Modulation of Adipocyte Differentiation and Proadipogenic Gene Expression by Sulforaphane, Genistein, and Docosahexaenoic Acid as a First Step to Counteract Obesity.

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Obesity is characterized by excess body fat accumulation due to an increase in the size and number of differentiated mature adipocytes. Adipocyte differentiation is regulated by genetic and environmental factors, and its inhibition could represent a strategy for obesity prevention and treatment. The

Sulforaphane induces adipocyte browning and promotes glucose and lipid utilization.

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Obesity is closely related to the imbalance of white adipose tissue storing excess calories, and brown adipose tissue dissipating energy to produce heat in mammals. Recent studies revealed that acquisition of brown characteristics by white adipocytes, termed "browning," may positively contribute to

Sulforaphane modulates CX3CL1/CX3CR1 axis and inflammation in palmitic acid-induced cell injury in C2C12 skeletal muscle cells

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Studies have shown that sulforaphane (SFN) has potent anti-inflammatory and free radical scavenging effects on obesity and associated disorder such as diabetes, polycystic ovary syndrome, and metabolic syndrome. fractalkine (CX3CL1) and its receptor, CX3CR1, play an important role in muscle

The Prevention of a High Dose of Vitamin D or Its Combination with Sulforaphane on Intestinal Inflammation and Tumorigenesis in Apc1638N Mice Fed a High-Fat Diet.

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METHODS The previous study shows that obesity-promoted inflammation is responsible for the activation of the intestinal tumorigenic Wnt-signaling. The present study aims to test a dietary strategy, dietary supplementation with a high dose of vitamin D (VD) or its combination with sulforaphane (SFN)

Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes.

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A potentially useful approach for drug discovery is to connect gene expression profiles of disease-affected tissues ("disease signatures") to drug signatures, but it remains to be shown whether it can be used to identify clinically relevant treatment options. We analyzed coexpression networks and

Concerted redox modulation by sulforaphane alleviates diabetes and cardiometabolic syndrome.

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Diabetes and cardiometabolic disorders such as hypertension and obesity are major risk factors for the development of cardiovascular disease, with a wealth of evidence suggesting that oxidative stress is linked to the initiation and pathogenesis of these disease processes. With yearly increases in

Pharmaconutrition for the obese, critically ill patient.

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Obesity is an epidemic that affects approximately 30% of the adult population in the United States. The prevalence of obesity in the critically ill seems to correlate with the rise in obesity in the general population. Delivery of standard enteral nutrition (EN) to patients in the intensive care

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