Morvarid Kabir (0000-0003-0880-3767)

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http://www.ncbi.nlm.nih.gov/myncbi/collections/mybibliography/
There is an abundance of evidence demonstrating the association of obesity, in particular central or intra-abdominal obesity, with a cluster of metabolic disorders. One of the research goals of our laboratory is to understand the molecular regulation of adipose tissue from different anatomical depots and why intra-abdominal obesity is associated with the whole body and hepatic insulin resistance. Recently, our group has also been interested in the role of reduced hepatic insulin clearance in Type 2 diabetes. We perform physiological, cellular, and molecular experiments to clarify whether reduced hepatic insulin clearance can lead to Type 2 diabetes. We utilize molecular and cellular techniques to examine the interplay between adipose tissue, liver, muscle, and heart during insulin resistance and obesity using interventions such as fat feeding and insulin-sensitizing drugs, including a selective endocannabinoid receptor antagonist and sodium-glucose cotransporter-2 (SGLT2) inhibitors. My group demonstrated the mechanisms by which CB1 antagonists and SGLT2 inhibitors promote being and improve energy homeostasis in adipose tissue.

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Cedars-Sinai Medical Center: Los Angeles, CA, US

2011-07-01 to present | Assistant Professor (Medicine/ Biomedical Sciences)

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Morvarid Kabir

https://orcid.org/0000-0003-0880-3767

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Employment (5)

Cedars-Sinai Medical Center: Los Angeles, CA, US

University of Southern California: Los Angeles, CA, US

University of Southern California: Los Angeles, CA, US

Universite Paris V Rene Decartes: Paris, FR

University of Southern California: Los Angeles, CA, US

Education and qualifications (3)

Université Pierre et Marie Curie: Paris, Île-de-France, FR

Université Pierre et Marie Curie: Paris, Île-de-France, FR

Universite Jussieu Paris 7: Paris, Île-de-France, FR

Professional activities (2)

Obesity Society: Silver Spring, Maryland, US

American Diabetes Association : Arlington, US

Works (42)

Editorial: Multifaceted cannabinoids: regulators of normal and pathological function in metabolic and endocrine organs, volume II

Dapagliflozin prevents abdominal visceral and subcutaneous adipose tissue dysfunction in the insulin‐resistant canine model

The Physiology of Insulin Clearance

Correction: Paszkiewicz et al. A Peripheral CB1R Antagonist Increases Lipolysis, Oxygen Consumption Rate, and Markers of Beiging in 3T3-L1 Adipocytes Similar to RIM, Suggesting That Central Effects Can Be Avoided. Int. J. Mol. Sci. 2020, 21, 6639

A Peripheral CB1R Antagonist Increases Lipolysis, Oxygen Consumption Rate, and Markers of Beiging in 3T3-L1 Adipocytes Similar to RIM, Suggesting that Central Effects Can Be Avoided

Novel Aspects of the Role of the Liver in Carbohydrate Metabolism

Hypothesis: Role of Reduced Hepatic Insulin Clearance in the Pathogenesis of Type 2 Diabetes.

Activation of NPRs and UCP1-independent pathway following CB1R antagonist treatment is associated with adipose tissue beiging in fat-fed male dogs.

Quantitative path to deep phenotyping: Possible importance of reduced hepatic insulin degradation to type 2 diabetes mellitus pathogenesis.

Variability of Directly Measured First-Pass Hepatic Insulin Extraction and Its Association With Insulin Sensitivity and Plasma Insulin.

Assessment of hepatic insulin extraction from in vivo surrogate methods of insulin clearance measurement.

Exenatide Treatment Alone Improves β-Cell Function in a Canine Model of Pre-Diabetes.

Renal Denervation Reverses Hepatic Insulin Resistance Induced by High-Fat Diet.

Corrections: High-Fat Diet-Induced Insulin Resistance does not Increase Plasma Anandamide Levels or Potentiate Anandamide Insulinotropic Effect in Isolated Canine Islets.

High-fat diet-induced insulin resistance does not increase plasma anandamide levels or potentiate anandamide insulinotropic effect in isolated canine islets.

CB1R antagonist increases hepatic insulin clearance in fat-fed dogs likely via upregulation of liver adiponectin receptors.

Increase in visceral fat per se does not induce insulin resistance in the canine model.

Failure of homeostatic model assessment of insulin resistance to detect marked diet-induced insulin resistance in dogs.

Hepatic insulin clearance is the primary determinant of insulin sensitivity in the normal dog.

CB(1) antagonism restores hepatic insulin sensitivity without normalization of adiposity in diet-induced obese dogs.

Simplified method to isolate highly pure canine pancreatic islets.

Large size cells in the visceral adipose depot predict insulin resistance in the canine model.

Novel canine models of obese prediabetes and mild type 2 diabetes.

Rimonabant prevents additional accumulation of visceral and subcutaneous fat during high-fat feeding in dogs.

Treatment for 2 mo with n 3 polyunsaturated fatty acids reduces adiposity and some atherogenic factors but does not improve insulin sensitivity in women with type 2 diabetes: a randomized controlled study.

Metabolic syndrome, hyperinsulinemia, and cancer.

Abdominal obesity: role in the pathophysiology of metabolic disease and cardiovascular risk.

Low glycemic index foods should play a role in improving overall glycemic control in type-1 and type-2 diabetic patients and, more specifically, in correcting excessive postprandial hyperglycemia.

Role of low-glycemic-index foods in improving overall glycemic control in type 1 and type 2 diabetic patients and correcting excessive postprandial hyperglycemia.

Why visceral fat is bad: mechanisms of the metabolic syndrome.

Metabolic dysregulation with atypical antipsychotics occurs in the absence of underlying disease: a placebo-controlled study of olanzapine and risperidone in dogs.

Molecular evidence supporting the portal theory: a causative link between visceral adiposity and hepatic insulin resistance.

Elevated glucagon-like peptide-1-(7-36)-amide, but not glucose, associated with hyperinsulinemic compensation for fat feeding.

Four-week low-glycemic index breakfast with a modest amount of soluble fibers in type 2 diabetic men.

Regulation of glucose transport and transporter 4 (GLUT-4) in muscle and adipocytes of sucrose-fed rats: effects of N-3 poly- and monounsaturated fatty acids.

Chronic consumption of fresh but not heated yogurt improves breath-hydrogen status and short-chain fatty acid profiles: a controlled study in healthy men with or without lactose maldigestion.

Negative regulation of leptin by chronic high-glycemic index starch diet.

35th Annual Meeting of the European Association for the Study of Diabetes : Brussels, Belgium, 28 September-2 October 1999.

A high glycemic index starch diet affects lipid storage-related enzymes in normal and to a lesser extent in diabetic rats.

Plasma lipids and fatty acid synthase activity are regulated by short-chain fructo-oligosaccharides in sucrose-fed insulin-resistant rats.

Dietary amylose-amylopectin starch content affects glucose and lipid metabolism in adipocytes of normal and diabetic rats.

Effects of long-term low-glycaemic index starchy food on plasma glucose and lipid concentrations and adipose tissue cellularity in normal and diabetic rats.

Peer review (1 review for 1 publication/grant)