Zucker Diabetic‐Sprague Dawley (ZDSD) rat: Type 2 diabetes translational research model

Wang, Andrea N.; Carlos, Joselia; Fraser, Graham M.; McGuire, John J.

doi:10.1113/ep089947

Cited by 21 publications

(17 citation statements)

References 100 publications

(258 reference statements)

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“…As their rats were approximately 130 g heavier at the start of the study, it is possible that the current starting weight of animals in our study was not yet sufficiently large enough to maximize metabolic dysregulation. Nevertheless, it will be important to test the effects of psilocybin using more complex paradigms of obesity and metabolic syndrome/diabetes, using models such as the Zucker rat ( 46 ) to assess the entirety of metabolic changes that might be improved.…”

Section: Discussionmentioning

confidence: 99%

Chronic Treatment With Psilocybin Decreases Changes in Body Weight in a Rodent Model of Obesity

et al. 2022

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BackgroundThere are currently relatively few effective pharmacological treatments for obesity, and existing ones may be associated with limiting side-effects. In the search for novel anti-obesity agents, drugs that modify central serotonergic systems have historically proven to be effective in promoting weight loss. Psilocin, which is rapidly metabolized from psilocybin, is an agonist at multiple serotonin receptors. In the present study we assessed the effects of psilocybin and a positive control (metformin) on changes in body weight in a rat model of obesity.MethodsFive groups of adult male rats were pre-conditioned with a cafeteria diet until obese (>600 g) and then treated with either psilocybin (0.1, 1, or 5 mg/kg, i.p.), metformin (300 mg/kg, p.o.) or vehicle control. Treatments were for 27 consecutive weekdays, and body weights and high calorie food intake were recorded daily. Fasting glucose levels were recorded after 11 days of treatment. At the end of treatment rats completed a glucose tolerance test, and multiple fat pads were dissected out to assess adiposity.ResultsThe medium dose psilocybin group had to be terminated from the study prematurely. Both the low and high dose psilocybin groups caused a significant decrease in changes in body weight compared to controls. The metformin group produced a greater decrease in change in body weight than either psilocybin groups or controls. Both high dose psilocybin and metformin decreased consumption of the high calorie diet, and exhibited decreased central adiposity.ConclusionPsilocybin demonstrated modest but significant effects on weight gain. Further study is recommended.

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Section: Discussionmentioning

confidence: 99%

Chronic Treatment With Psilocybin Decreases Changes in Body Weight in a Rodent Model of Obesity

et al. 2022

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Section: Discussionmentioning

confidence: 99%

“…These studies are not without limitations as they were performed in a rodent model of type 2 diabetes and therefore mimic but do not include all the characteristics and pathways associated with human type 2 diabetes 30,31 Our ischemia-reperfusion model used a temporary ligation of the LAD with 30 min of warm ischemia time. This time was adopted to ensure animal survival in our vehicle alone group and therefore longer ischemic times would be required for validation in patients ischemia may be prolonged.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic and proteomic pathways of diabetic and non-diabetic mitochondrial transplantation

Doulamis

Nomoto

Tzani

et al. 2022

Sci Rep

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Reduced mitochondrial function increases myocardial susceptibility to ischemia–reperfusion injury (IRI) in diabetic hearts. Mitochondrial transplantation (MT) ameliorates IRI, however, the cardioprotective effects of MT may be limited using diabetic mitochondria. Zucker Diabetic Fatty (ZDF) rats were subjected to temporary myocardial RI and then received either vehicle alone or vehicle containing mitochondria isolated from either diabetic ZDF or non-diabetic Zucker lean (ZL) rats. The ZDF rats were allowed to recover for 2 h or 28 days. MT using either ZDF- or ZL-mitochondria provided sustained reduction in infarct size and was associated with overlapping upregulation of pathways associated with muscle contraction, development, organization, and anti-apoptosis. MT using either ZDF- or ZL-mitochondria also significantly preserved myocardial function, however, ZL- mitochondria provided a more robust long-term preservation of myocardial function through the mitochondria dependent upregulation of pathways for cardiac and muscle metabolism and development. MT using either diabetic or non-diabetic mitochondria decreased infarct size and preserved functional recovery, however, the cardioprotection afforded by MT was attenuated in hearts receiving diabetic compared to non-diabetic MT.

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“…The Zucker Diabetic Sprague–Dawley (ZDSD) rat is another model for experimental studies of T2DM, with a characteristic phenotype that is independent of leptin receptor signaling [ 191 ]. This rat does not carry the leptin receptor mutation ( fa / fa ) and develops a prediabetic state that progresses to overt diabetes with age, with common morbidities, such as cardiomyopathy, that are associated with an increased risk occurrence in prediabetic patients.…”

Section: Functionality Of Leptin and Its Involvement In Pathologymentioning

confidence: 99%

Recent Advances in the Knowledge of the Mechanisms of Leptin Physiology and Actions in Neurological and Metabolic Pathologies

Casado

Collado-Pérez

Frago

et al. 2023

IJMS

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Excess body weight is frequently associated with low-grade inflammation. Evidence indicates a relationship between obesity and cancer, as well as with other diseases, such as diabetes and non-alcoholic fatty liver disease, in which inflammation and the actions of various adipokines play a role in the pathological mechanisms involved in these disorders. Leptin is mainly produced by adipose tissue in proportion to fat stores, but it is also synthesized in other organs, where leptin receptors are expressed. This hormone performs numerous actions in the brain, mainly related to the control of energy homeostasis. It is also involved in neurogenesis and neuroprotection, and central leptin resistance is related to some neurological disorders, e.g., Parkinson’s and Alzheimer’s diseases. In peripheral tissues, leptin is implicated in the regulation of metabolism, as well as of bone density and muscle mass. All these actions can be affected by changes in leptin levels and the mechanisms associated with resistance to this hormone. This review will present recent advances in the molecular mechanisms of leptin action and their underlying roles in pathological situations, which may be of interest for revealing new approaches for the treatment of diseases where the actions of this adipokine might be compromised.

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Zucker Diabetic‐Sprague Dawley (ZDSD) rat: Type 2 diabetes translational research model

Cited by 21 publications

References 100 publications

Chronic Treatment With Psilocybin Decreases Changes in Body Weight in a Rodent Model of Obesity

Chronic Treatment With Psilocybin Decreases Changes in Body Weight in a Rodent Model of Obesity

Transcriptomic and proteomic pathways of diabetic and non-diabetic mitochondrial transplantation

Recent Advances in the Knowledge of the Mechanisms of Leptin Physiology and Actions in Neurological and Metabolic Pathologies

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