Sexual dimorphism exists to a small degree at birth, but striking differences develop during the pubertal years. The development of this dimorphism in body composition is largely regulated by endocrine factors, with critical roles played by growth hormone and gonadal steroids. It is important for clinicians and researchers to know the normal changes in order to address pathologic findings in disease states.

Diabetes mellitus (DM) is a common spontaneous endocrine disorder in dogs, which is defined by persistent hyperglycemia and insulin deficiency. Like type 1 diabetes (T1D) in people, canine DM is a complex and multifactorial disease in which genomic and epigenomic factors interact with environmental cues to induce pancreatic β‐cell loss and insulin deficiency, although the pathogenesis of canine DM is poorly defined and the role of autoimmunity is further controversial. Both diseases are incurable and require life‐long exogenous insulin therapy to maintain glucose homeostasis. Human pancreatic islet physiology, size, and cellular composition is further mirrored by canine islets. Although pancreatic or isolated islets transplantation are the only clinically validated methods to achieve long‐term normoglycemia and insulin independence, their availability does not meet the clinical need; they target a small portion of patients and have significant potential adverse effects. Therefore, providing a new source for β‐cell replacement is an unmet need. Naturally occurring DM in pet dogs, as a translational platform, is an untapped resource for various regenerative medicine applications that may offer some unique advantages given dogs' large size, longevity, heterogenic genetic background, similarity to human physiology and pathology, and long‐term clinical management. In this review, we outline different strategies for curative approaches, animal models used, and consider the value of canine DM as a translational animal/disease model for T1D in people. stem cells translational medicine 2019;8:450–455

A 1670-g male infant was born by emergent cesarean section at 32 and 5/7 weeks' gestation caused by nonreassuring fetal heart rate tracings. The patient's mother was a 25-year-old gravida 1 woman with a history of Graves disease (antithyroid peroxidase [APO] antibody positive at 208 IU/mL) and hypothyroidism secondary to radioiodine ablation performed 2 years before the delivery. Her thyroid studies were normal throughout pregnancy, with the exception of a mildly elevated thyroid-stimulating hormone level of 12 mIU/mL obtained during the third trimester. The pregnancy was further complicated by type 1 diabetes mellitus and drug, tobacco, and alcohol use. A fetal echocardiogram revealed a constricted ductus arteriosus, right ventricular hypertrophy, right atrial enlargement, and tricuspid regurgitation.After birth, the infant was intubated for poor respiratory effort and concern for underlying heart disease. He also developed early thrombocytopenia requiring platelet transfusion. Other early laboratory values showed hypoglycemia, evidence of disseminated intravascular coagulopathy, and elevated neonatal bilirubin (Table 1). On day of life (DOL) 2, the patient was jaundiced (conjugated bilirubin level of 11.2 mg/dL). Liver enzymes and alkaline phosphatase concentrations were elevated (Table 1). Doppler ultrasound excluded anatomic anomalies of the biliary tree and gallbladder. Serum tests for toxoplasmosis, rubella, cytomegalovirus, and herpes simplex virus were negative, as were bacterial cultures of urine and blood. Metabolic studies, including those for a 1 -antitrypsin deficiency, were normal. The patient received fresh frozen plasma and platelet concentrate and his coagulopathy resolved, as did respiratory distress.On DOL 4, the patient became hypertensive and tachycardic (heart rate 235 bpm), prompting evaluation of his thyroid status. On DOL 5, he was diagnosed with thyrotoxicosis (Table 1). He was started on propylthiouracil (PTU) and propranolol on DOL 6, and heart rate and blood pressure normalized within 24 hours. His conjugated bilirubin concentration decreased following initiation of therapy on DOL 6. Given the lower incidence of hepatatoxicity with methimazole (MMI) compared with PTU in children (1), PTU was discontinued after 6 doses and therapy with MMI initiated on DOL 7; however, the patient's transaminase levels increased further while on MMI therapy, peaking at an aspartate aminotransferase concentration of 601 U/L and an alanine transaminase concentration of 190 U/L on DOL 17; thus, MMI was discontinued.Hyperthyroidism did not recur and the patient became euthyroid soon after (Table 1).The infant was diagnosed postnatally with mild pulmonary hypertension (pulmonary artery pressure two-thirds of systemic pressure), believed to be secondary to ductus arteriosus constriction in utero, requiring no postnatal intervention. Follow-up echocardiograms revealed no significant pathology.The patient was discharged on DOL 24. Outpatient follow-up showed improving cholestasis with a conjugated bilirubin co...

Puberty is a complex process of developmental change regulated by multiple genetic and endocrine controls. Abnormal pubertal development (both precocious and delayed puberty) can cause significant distress to the patient and may in some instances be a sign of life-threatening pathology. Delayed puberty is often due to constitutional delay of growth and puberty, but will also occur in cases of primary gonadal failure and in patients with disorders leading to diminished gonadotropin levels (ie, central nervous system [CNS] tumors). Precocious puberty may occur due to CNS disorders, certain genetic disorders, ectopic gonadotropin secretion or autonomous sex steroid secretion. Treatment is directed toward the underlying pathology, and may include agents to either stimulate or block pubertal development. Health care providers require knowledge of the normal onset of timing and rate of progression of puberty, and must be able to identify patients with abnormal pubertal development, as well as initiate the appropriate laboratory workup.