Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...
Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
Chronic Kidney Disease I: Introduction01:25

Chronic Kidney Disease I: Introduction

Chronic Kidney Disease (CKD) arises when the kidneys progressively lose their ability to function, ultimately leading to end-stage renal disease. At this advanced stage, the kidneys can no longer filter waste or maintain essential body functions, requiring renal replacement therapy (RRT) through dialysis or a kidney transplant for survival.Early-stage chronic kidney disease and detection challengesIn CKD's early stages, symptoms often remain absent because healthy nephrons compensate for...
Diabetic Ketoacidosis ll: Pathophysiology01:22

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

CD59 drives diet-induced obesity and glucose intolerance, insulin resistance, and metabolic dysfunction-associated steatotic liver disease.

npj metabolic health and disease·2026
Same author

Intractable dialysis-associated headache: a management dilemma in pediatric hemodialysis.

Pediatric nephrology (Berlin, Germany)·2026
Same author

Cannabidiol and cannabigerol ameliorate steatotic liver disease via phosphocreatine buffering and lysosomal restoration.

British journal of pharmacology·2026
Same author

Corrigendum to "The paradoxical protective effect of chronic stress on advanced Alzheimer's disease pathology". [Brain, Behav., Immun. 132 (2026) 106224].

Brain, behavior, and immunity·2026
Same author

Colloid-patterned surfaces distinguish malignant mechanophenotypes.

Materials today. Bio·2026
Same author

The paradoxical protective effect of chronic stress on advanced Alzheimer's disease pathology.

Brain, behavior, and immunity·2025

Related Experiment Video

Updated: May 8, 2026

Monitoring Blood Glucose in Mouse Offspring After Intracytoplasmic Sperm Injection
06:11

Monitoring Blood Glucose in Mouse Offspring After Intracytoplasmic Sperm Injection

Published on: May 17, 2024

Gestational Ketosis Compromises Nephron Endowment and Long-Term Kidney Function in Offspring.

Athar Amleh1,2, Yaniv Makayes1,2, Eden Abergel1,2

  • 1Pediatric Nephrology Unit, Hadassah Medical Center and Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel.

Journal of the American Society of Nephrology : JASN
|May 6, 2026
PubMed
Summary

Maternal ketosis from ketogenic diets or supplements reduces offspring nephron number, impairing kidney function. This congenital deficit persists despite postnatal recovery, highlighting risks to fetal kidney development.

Keywords:
CKDcell signalingchildrenmetabolismnephron developmentnutritionpediatric nephrologyrenal development

More Related Videos

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats
05:34

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats

Published on: April 4, 2025

Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure
10:07

Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure

Published on: March 20, 2012

Related Experiment Videos

Last Updated: May 8, 2026

Monitoring Blood Glucose in Mouse Offspring After Intracytoplasmic Sperm Injection
06:11

Monitoring Blood Glucose in Mouse Offspring After Intracytoplasmic Sperm Injection

Published on: May 17, 2024

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats
05:34

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats

Published on: April 4, 2025

Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure
10:07

Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure

Published on: March 20, 2012

Area of Science:

  • Reproductive biology
  • Developmental biology
  • Nephrology

Background:

  • Ketogenic diets are increasingly popular, raising safety concerns during pregnancy.
  • While mild ketosis is normal in pregnancy, the effects of diet-induced ketosis on fetal kidney development are unknown.
  • This study investigates maternal ketosis' impact on offspring nephrogenesis and long-term kidney outcomes.

Purpose of the Study:

  • To determine the effects of maternal ketosis on fetal kidney development and nephrogenesis.
  • To assess the long-term kidney function in offspring exposed to maternal ketosis.
  • To elucidate the molecular mechanisms underlying ketosis-induced nephrogenesis disruption.

Main Methods:

  • Utilized two murine models: maternal ketogenic diet and β-hydroxybutyrate supplementation throughout gestation.
  • Assessed offspring kidney structure and function via nephron counts, kidney size, and serum markers.
  • Examined nephron progenitor cell (NPC) dynamics using transcriptomics, immunostaining, and qPCR.

Main Results:

  • Both ketogenic diet and β-hydroxybutyrate supplementation reduced offspring nephron number and impaired kidney function.
  • Transcriptomic analysis revealed suppressed cell-cycle and Myc signaling, with activated inflammatory pathways (TNFα/NFκB) in NPCs.
  • Reduced NPC proliferation and c-Myc, increased TNFα expression, and insufficient postnatal recovery confirmed a nephron deficit.

Conclusions:

  • Maternal ketosis disrupts fetal kidney development by suppressing c-Myc signaling and activating NPC inflammation.
  • This leads to a congenital nephron deficit and compromised adult kidney function.
  • Findings highlight potential risks of ketogenic diets during pregnancy for offspring kidney health.