Gestational Diabetes Mellitus

Gestational diabetes mellitus (GDM) is a form of carbohydrate intolerance that is first recognized during pregnancy and typically resolves after parturition. In veterinary medicine, GDM is a rare but documented endocrinopathy of the bitch and queen, characterized by transient hyperglycemia, glucosuria, and insulin resistance that develops in the second half of gestation due to the diabetogenic effects of placental hormones, particularly progesterone and growth hormone. Unlike type I diabetes mellitus, which results from absolute insulin deficiency, GDM is a state of relative insulin insufficiency where pancreatic beta-cell function cannot compensate for the increased insulin resistance induced by pregnancy. The condition is analogous to human GDM and poses significant risks to both the dam and the developing fetuses, including macrosomia, fetal hypoxia, and increased neonatal mortality. In the bitch, the corpus luteum is the primary source of progesterone throughout gestation, and progesterone levels peak around day 30-40, coinciding with the onset of insulin resistance. In the queen, placental lactogen and growth hormone contribute to the metabolic alterations. GDM must be distinguished from pre-existing diabetes mellitus that is unmasked by pregnancy, and from transient diabetes secondary to diestrus (progesterone-induced) in non-pregnant bitches. Accurate diagnosis requires serial blood glucose measurements, fructosamine levels, and careful monitoring of pregnancy progression. Management involves dietary modification, insulin therapy, and close obstetric monitoring to optimize maternal and fetal outcomes.

The primary etiology of gestational diabetes mellitus in dogs and cats is the physiological insulin resistance that occurs during pregnancy, driven by hormonal changes. In the bitch, the corpus luteum secretes high levels of progesterone, which is known to induce insulin resistance by decreasing insulin receptor sensitivity and impairing glucose uptake in peripheral tissues. Progesterone also stimulates the secretion of growth hormone from the mammary gland, which further exacerbates insulin resistance. In the queen, placental lactogen and growth hormone are the main diabetogenic hormones. Additionally, increased levels of cortisol and prolactin during pregnancy contribute to the metabolic stress. Genetic predisposition may play a role, as certain breeds (e.g., Miniature Poodles, Dachshunds) are more prone to diabetes mellitus, and a history of previous GDM increases the risk. Obesity and advanced maternal age are significant risk factors. In some cases, GDM may be triggered by exogenous corticosteroid administration during pregnancy, which can induce insulin resistance. Pancreatic beta-cell dysfunction, whether due to inadequate beta-cell mass or impaired insulin secretion, is a prerequisite for the development of overt hyperglycemia. The exact molecular mechanisms involve downregulation of GLUT4 transporters, increased hepatic gluconeogenesis, and altered adipokine secretion (e.g., increased resistin, decreased adiponectin). In rare instances, GDM may be associated with underlying subclinical pancreatitis or autoimmune insulitis. Iatrogenic causes include inappropriate use of progestins for pregnancy maintenance, which can precipitate insulin resistance.

Gestational diabetes mellitus is a rare condition in small animal practice, with limited epidemiological data. In dogs, the incidence is estimated to be less than 1% of pregnancies, but it may be underdiagnosed due to lack of routine screening. Certain breeds appear to be overrepresented, including Miniature Poodles, Dachshunds, and Beagles, which are also predisposed to diabetes mellitus in general. Older bitches (over 6 years of age) and those with a history of obesity or previous GDM are at higher risk. In cats, GDM is even rarer, but domestic shorthair and longhair cats may be affected. There is no clear sex predilection as the condition is exclusive to pregnant females. Parity may influence risk, with primigravid animals possibly being more susceptible due to hormonal fluctuations. The condition is more likely to be diagnosed in the second half of gestation (days 35-60 in dogs, days 30-55 in cats), corresponding to peak progesterone and placental hormone levels. Breed-specific genetic factors may affect insulin sensitivity and pancreatic beta-cell reserve. Environmental factors such as overfeeding and lack of exercise during pregnancy contribute to the risk. In a retrospective study of canine diabetes, GDM accounted for approximately 5% of all diabetes cases in intact bitches. The true prevalence may be higher as transient hyperglycemia may go unnoticed without routine glucose monitoring.

The pathophysiology of gestational diabetes mellitus involves a complex interplay of hormonal, metabolic, and cellular changes. During pregnancy, the placenta and corpus luteum produce hormones that antagonize insulin action, leading to progressive insulin resistance. In the bitch, progesterone levels rise from day 15 and peak around day 30-40, with concentrations often exceeding 20 ng/mL. Progesterone reduces the expression and translocation of GLUT4 glucose transporters in skeletal muscle and adipose tissue, impairing glucose uptake. It also enhances hepatic gluconeogenesis and glycogenolysis, increasing glucose output. Growth hormone, secreted by the mammary gland under the influence of progesterone, further promotes lipolysis and insulin resistance. In the queen, placental lactogen and growth hormone are the primary diabetogenic factors. As pregnancy advances, the increasing demands of the fetoplacental unit for glucose, amino acids, and other nutrients place additional stress on the maternal pancreas. In a normal pregnancy, pancreatic beta-cells undergo hyperplasia and increase insulin secretion to compensate for insulin resistance. In GDM, this compensatory mechanism fails, resulting in relative insulin deficiency and hyperglycemia. Hyperglycemia leads to glucosuria when the renal threshold for glucose is exceeded (approximately 180-220 mg/dL in dogs and cats), causing osmotic diuresis and polyuria. Chronic hyperglycemia can cause fetal hyperinsulinemia, leading to macrosomia, organomegaly, and increased oxygen consumption, which may result in fetal hypoxia and acidosis. In the dam, prolonged hyperglycemia can lead to ketosis, hepatic lipidosis, and increased susceptibility to infections. The exact cellular mechanisms involve impaired insulin signaling via IRS-1 and PI3K pathways, increased expression of protein tyrosine phosphatases, and altered adipokine profiles. Oxidative stress and inflammation also contribute to beta-cell dysfunction.

Several intrinsic and extrinsic factors predispose a pregnant bitch or queen to gestational diabetes mellitus. Intrinsic factors include genetic predisposition, as certain breeds (e.g., Miniature Poodle, Dachshund, Beagle) have a higher baseline risk for diabetes mellitus. Age is a significant factor, with older animals (greater than 6 years) being more susceptible. Obesity is a major risk factor, as adipose tissue secretes pro-inflammatory cytokines and adipokines that promote insulin resistance. Parity may play a role, with primigravid animals possibly at higher risk due to hormonal fluctuations. A history of previous GDM or a family history of diabetes increases the likelihood. Underlying subclinical pancreatic insufficiency or autoimmune insulitis can predispose to GDM. Extrinsic factors include exogenous corticosteroid administration during pregnancy, which can induce insulin resistance. Inappropriate use of progestins (e.g., megestrol acetate) for pregnancy maintenance can also precipitate GDM. Nutritional factors, such as a high-carbohydrate diet or overfeeding, contribute to hyperglycemia. Stress, whether from environmental changes or concurrent illness, can elevate cortisol levels and exacerbate insulin resistance. Lack of exercise during pregnancy may also increase the risk. In cats, obesity and a sedentary lifestyle are particularly important. Additionally, certain medications, such as diuretics or beta-agonists, may impair glucose tolerance. Breed-specific anatomical factors, such as a small body size with a large litter, may increase metabolic demands and stress.

The clinical signs of gestational diabetes mellitus typically appear in the second half of pregnancy and may be subtle initially. The most common signs are polyuria, polydipsia, and polyphagia, which are often attributed to pregnancy itself. Weight loss may occur despite a good appetite, due to the catabolic state. Lethargy and weakness are common. In some cases, owners may notice a sweet or fruity odor to the breath, indicating ketonemia. As the condition progresses, signs of dehydration may develop, including dry mucous membranes and decreased skin turgor. In severe cases, vomiting, diarrhea, and anorexia may occur, leading to ketoacidosis. Physical examination may reveal a dull hair coat, poor body condition, and signs of dehydration. Abdominal palpation may reveal large fetuses (macrosomia) or polyhydramnios. In the bitch, vaginal discharge may be normal, but if secondary infection occurs, purulent discharge may be present. In the queen, similar signs are observed. Neurological signs such as hindlimb weakness or plantigrade stance may occur in cats with diabetic neuropathy, though this is more common in chronic diabetes. Ophthalmic examination may reveal cataracts in chronic cases, but this is rare in GDM. The presence of concurrent urinary tract infections is common due to glucosuria. If left untreated, GDM can progress to diabetic ketoacidosis, which presents with severe depression, dehydration, tachypnea, and a characteristic acetone odor. Fetal distress may manifest as decreased fetal movements or stillbirths. It is important to note that clinical signs may be mild and easily overlooked, emphasizing the need for routine glucose screening in high-risk pregnancies.

The differential diagnoses for gestational diabetes mellitus include other causes of hyperglycemia and polyuria/polydipsia in pregnant animals. These include: 1) Pre-existing diabetes mellitus (Type I or Type II) that is unmasked by pregnancy; this can be differentiated by a history of hyperglycemia prior to pregnancy or by elevated fructosamine levels indicating chronic hyperglycemia. 2) Diestrus-associated diabetes mellitus in non-pregnant bitches, which is caused by high progesterone levels during diestrus; this can be ruled out by confirming pregnancy via ultrasonography. 3) Transient hyperglycemia due to stress, which is common in cats; this can be differentiated by measuring fructosamine or by performing a glucose tolerance test. 4) Acromegaly, caused by growth hormone-secreting pituitary tumors, which can occur in cats and dogs; this is rare and may be associated with insulin resistance and other signs such as prognathia inferior. 5) Hyperadrenocorticism (Cushing's syndrome), which can cause insulin resistance and hyperglycemia; this is more common in dogs and can be diagnosed with ACTH stimulation or low-dose dexamethasone suppression tests. 6) Pancreatitis, which can cause transient or permanent diabetes; this is often associated with abdominal pain, vomiting, and elevated pancreatic lipase. 7) Urinary tract infection, which can cause polyuria and polydipsia but is not typically associated with hyperglycemia; urinalysis and culture are diagnostic. 8) Renal glucosuria, which is a benign condition with glucosuria but normal blood glucose; this can be differentiated by blood glucose measurement. 9) Drug-induced hyperglycemia, such as from corticosteroids or progestins; this can be ruled out by history. 10) Hepatic lipidosis, which can cause hyperglycemia in cats but is more commonly associated with anorexia and jaundice. A thorough diagnostic workup is essential to differentiate these conditions.

The diagnostic algorithm for gestational diabetes mellitus begins with a thorough history and physical examination, focusing on risk factors and clinical signs. If GDM is suspected, the following steps are recommended: 1) Confirm pregnancy via abdominal ultrasonography or palpation (after day 25-30). 2) Measure fasting blood glucose; a value greater than 110 mg/dL in dogs or 120 mg/dL in cats is suspicious, but a single elevated reading may be due to stress. 3) Perform a serum fructosamine concentration; fructosamine reflects average glucose levels over the past 1-2 weeks and is not affected by acute stress. A fructosamine level above the reference range (typically >350 µmol/L in dogs, >400 µmol/L in cats) supports a diagnosis of diabetes. 4) If fructosamine is equivocal, perform a glucose tolerance test: administer 1 g/kg of glucose intravenously and measure blood glucose at 0, 30, 60, 90, and 120 minutes. In normal pregnancy, glucose returns to baseline within 60-90 minutes; in GDM, there is a delayed return. 5) Perform a complete urinalysis to detect glucosuria and ketonuria. 6) Evaluate for concurrent conditions such as urinary tract infection via urine culture. 7) Monitor blood glucose curves over a 12-24 hour period to assess the degree of hyperglycemia and guide insulin therapy. 8) Assess fetal well-being via ultrasonography, including fetal heart rate and fetal size. 9) Rule out other causes of hyperglycemia as listed in differential diagnoses. 10) If ketoacidosis is suspected, measure blood beta-hydroxybutyrate and blood gas analysis. The diagnosis of GDM is confirmed if hyperglycemia resolves after parturition. It is important to note that routine screening for GDM is not standard in veterinary practice, but it should be considered in high-risk pregnancies.

Laboratory findings in gestational diabetes mellitus include hyperglycemia, glucosuria, and ketonuria. Fasting blood glucose is typically elevated above 110 mg/dL in dogs and 120 mg/dL in cats, but may be normal in early stages. Serum fructosamine is elevated (>350 µmol/L in dogs, >400 µmol/L in cats), indicating chronic hyperglycemia. Glycosylated hemoglobin (HbA1c) may also be elevated, but fructosamine is more commonly used. Urinalysis reveals glucosuria (4+ on dipstick) and possibly ketonuria. Hematology may show a stress leukogram (neutrophilia, lymphopenia, eosinopenia) or signs of infection if concurrent urinary tract infection is present. Biochemistry may reveal elevated liver enzymes (ALT, ALP) due to hepatic lipidosis, and elevated triglycerides and cholesterol. In cases of ketoacidosis, there is metabolic acidosis with decreased bicarbonate, elevated beta-hydroxybutyrate, and electrolyte imbalances (hypokalemia, hyponatremia, hypophosphatemia). Serum progesterone levels are elevated (typically >10 ng/mL in dogs) and may be used to confirm pregnancy and assess luteal function. Insulin levels may be low or inappropriately normal relative to the hyperglycemia. Vaginal cytology is not typically performed for GDM diagnosis, but if performed, it may show changes consistent with pregnancy (e.g., superficial cells, no neutrophils). Uterine culture may be indicated if there is suspicion of infection. In summary, the key laboratory findings are persistent hyperglycemia, glucosuria, and elevated fructosamine.

Imaging plays a crucial role in the diagnosis and monitoring of gestational diabetes mellitus. Abdominal ultrasonography is the primary imaging modality. In GDM, ultrasonography may reveal large-for-gestational-age fetuses (macrosomia), which can be assessed by measuring fetal biparietal diameter (BPD) and comparing to reference ranges for the breed. Fetal heart rate (FHR) is an important indicator of fetal well-being; normal FHR in dogs is 180-220 beats per minute (bpm) in early gestation, decreasing to 140-180 bpm near term. In GDM, FHR may be elevated (>220 bpm) due to fetal hyperinsulinemia and hypoxia, or may be decreased (<160 bpm) in cases of fetal distress. The fetal-maternal interface may show thickening of the uterine wall or increased placental echogenicity. Polyhydramnios (excessive amniotic fluid) may be observed, which is a sign of fetal polyuria. The fetal bladder may be prominent due to glucosuria. In the dam, the liver may appear hyperechoic if hepatic lipidosis is present. Radiography is less useful for soft tissue evaluation but can be used to confirm pregnancy after day 42-45 when fetal skeletal mineralization is visible. Radiographs may show large fetal skeletons or fetal gas patterns in cases of fetal death. CT and MRI are rarely used but may be helpful in evaluating the pancreas or pituitary gland if acromegaly is suspected. Vaginoscopy is not indicated for GDM but may be used to assess vaginal discharge if infection is present. Doppler ultrasonography can be used to assess uterine artery blood flow, which may be altered in GDM. Overall, ultrasonography is essential for monitoring fetal well-being and guiding the timing of delivery.

Cytology and histopathology are not commonly used for the diagnosis of gestational diabetes mellitus, but they may be helpful in certain situations. Vaginal cytology can be performed to confirm pregnancy and assess the stage of the estrous cycle. In pregnancy, vaginal cytology typically shows a mixture of intermediate and superficial cells, with no neutrophils. However, this is not specific for GDM. Fine-needle aspiration of the pancreas may be performed if pancreatitis or pancreatic neoplasia is suspected, but this is rarely indicated. Histopathology of the pancreas may reveal beta-cell vacuolation or islet hyperplasia, but this is only possible post-mortem. In cases of concurrent urinary tract infection, urine cytology may show bacteria and inflammatory cells. If a cesarean section is performed, histopathology of the placenta may be evaluated; in GDM, the placenta may show villous edema, increased vascularity, and thickening of the basement membrane. These findings are similar to those in human GDM. In the liver, histopathology may reveal hepatic lipidosis, characterized by vacuolation of hepatocytes with fat. In cases of diabetic ketoacidosis, renal histopathology may show glycogen nephrosis. However, these findings are not specific to GDM and are rarely used in clinical practice. The diagnosis of GDM is primarily based on clinical signs, blood glucose, and fructosamine levels, and histopathology is not typically required.

The treatment of gestational diabetes mellitus in dogs and cats involves a multi-modal approach aimed at controlling hyperglycemia, managing pregnancy, and ensuring the health of the dam and fetuses. The primary goals are to maintain blood glucose levels within an acceptable range (80-150 mg/dL in dogs, 80-120 mg/dL in cats) while avoiding hypoglycemia, and to support the pregnancy to term. Treatment should be initiated as soon as the diagnosis is confirmed. The first step is dietary modification: a high-fiber, complex-carbohydrate diet is recommended to slow glucose absorption. In dogs, a diet with moderate fat and high insoluble fiber is often used; in cats, a low-carbohydrate, high-protein diet is preferred. Small, frequent meals (3-4 times daily) can help stabilize blood glucose. If dietary management alone is insufficient, insulin therapy is indicated. In dogs, NPH insulin (isophane insulin) is commonly used, starting at a dose of 0.25-0.5 U/kg subcutaneously every 12 hours. In cats, glargine or detemir insulin may be used, starting at 0.25 U/kg every 12 hours. The dose is adjusted based on serial blood glucose curves. Oral hypoglycemic agents such as glipizide are not recommended in dogs but may be used in cats, though insulin is preferred. In cases of diabetic ketoacidosis, aggressive fluid therapy with 0.9% sodium chloride, regular insulin (0.1 U/kg IV bolus, then 0.05-0.1 U/kg/hour CRI), and potassium supplementation are required. Concurrent infections, especially urinary tract infections, should be treated with appropriate antibiotics (e.g., amoxicillin-clavulanate 12.5-25 mg/kg PO q8h). Monitoring of fetal well-being is essential; if fetal distress is detected, early cesarean section may be indicated. After parturition, insulin requirements typically decrease dramatically, and insulin therapy may be discontinued within 24-48 hours. However, some animals may develop permanent diabetes mellitus. In such cases, long-term insulin therapy is required. Supportive care includes ensuring adequate hydration and nutrition, and monitoring for hypoglycemia during labor and postpartum.

The prognosis for gestational diabetes mellitus in dogs and cats is generally good if the condition is diagnosed early and managed appropriately. With proper insulin therapy and dietary management, most pregnancies can be carried to term, and the fetuses can be delivered successfully. However, there are risks to both the dam and the fetuses. Maternal complications include diabetic ketoacidosis, which can be life-threatening, and an increased risk of urinary tract infections and other infections. Fetal complications include macrosomia, which can lead to dystocia, and fetal hypoxia, which can result in stillbirth or neonatal death. The perinatal mortality rate in GDM is reported to be higher than in normal pregnancies, but with intensive monitoring, it can be reduced. After parturition, insulin requirements usually decrease rapidly, and many animals become euglycemic without insulin. However, some animals may develop permanent diabetes mellitus, especially if there is underlying pancreatic pathology. The recurrence rate of GDM in subsequent pregnancies is high, and affected animals should be monitored closely in future pregnancies. The long-term prognosis for the dam is good if she does not develop permanent diabetes. For the offspring, there is an increased risk of obesity and diabetes later in life, but this is not well-documented in veterinary medicine. Negative prognostic indicators include severe hyperglycemia at diagnosis, ketoacidosis, and poor response to insulin therapy. Overall, with early diagnosis and aggressive management, the prognosis is favorable.

Follow-up care for gestational diabetes mellitus is crucial to ensure the health of the dam and to monitor for the resolution or persistence of diabetes. After diagnosis, blood glucose should be monitored frequently, initially with serial blood glucose curves (every 2-4 hours for 12-24 hours) to adjust insulin doses. Once stable, blood glucose can be monitored every 1-2 weeks. Fructosamine levels should be rechecked every 2-4 weeks to assess long-term glycemic control. Fetal well-being should be monitored via ultrasonography every 1-2 weeks, including fetal heart rate, fetal size, and amniotic fluid volume. If fetal distress is detected, early delivery may be necessary. During labor, blood glucose should be monitored closely, as insulin requirements may change. After parturition, insulin therapy should be tapered and discontinued if blood glucose remains normal. Blood glucose should be rechecked 24-48 hours postpartum and then weekly for the first month. If hyperglycemia persists, a diagnosis of permanent diabetes mellitus should be made, and long-term insulin therapy initiated. The dam should be monitored for signs of hypoglycemia, especially if insulin is continued. A complete blood count and biochemistry panel should be repeated 2-4 weeks postpartum to assess for resolution of any metabolic abnormalities. Urinalysis and urine culture should be performed to rule out urinary tract infection. For future pregnancies, the dam should be screened for GDM early in gestation, and a glucose tolerance test may be recommended. Breeding of affected animals should be carefully considered, as GDM may recur. Overall, close follow-up is essential for optimal outcomes.

Clinical pearls: 1) Always consider GDM in any pregnant bitch or queen presenting with polyuria, polydipsia, or polyphagia, especially in the second half of gestation. 2) Fructosamine is the most reliable test to differentiate stress hyperglycemia from true diabetes, as it reflects average glucose over 1-2 weeks. 3) Insulin requirements may decrease dramatically after parturition; be prepared to reduce or discontinue insulin to avoid hypoglycemia. 4) Fetal heart rate is a critical indicator of fetal well-being; a rate below 160 bpm in dogs indicates fetal distress and may necessitate cesarean section. 5) Dietary management is the cornerstone of therapy; a high-fiber diet in dogs and a low-carbohydrate diet in cats can significantly improve glycemic control. 6) Monitor for concurrent urinary tract infections, which are common due to glucosuria. 7) In cats, stress hyperglycemia is common; always confirm with fructosamine before diagnosing GDM. Pitfalls: 1) Failing to screen for GDM in high-risk pregnancies, leading to delayed diagnosis and poor outcomes. 2) Using a single blood glucose measurement to diagnose GDM, which may be falsely elevated due to stress. 3) Overdosing insulin, leading to hypoglycemia, which can be fatal. 4) Neglecting to monitor fetal well-being, resulting in undetected fetal distress and stillbirth. 5) Assuming that hyperglycemia will resolve after parturition without monitoring, leading to missed cases of permanent diabetes. 6) Using oral hypoglycemic agents in dogs, which are ineffective and may be harmful. 7) Failing to adjust insulin doses based on serial blood glucose curves, leading to poor glycemic control. 8) Not considering other causes of hyperglycemia, such as acromegaly or hyperadrenocorticism, which may require different treatment.

The following drug protocols are based on Plumb's Veterinary Drug Handbook and current theriogenology guidelines. For insulin therapy in dogs: NPH insulin (Humulin N, Novolin N) is the first choice. Initial dose: 0.25-0.5 U/kg subcutaneously every 12 hours. Adjust dose by 10-20% based on blood glucose curves. For cats: Glargine (Lantus) or Detemir (Levemir) is preferred. Initial dose: 0.25 U/kg subcutaneously every 12 hours. Adjust as needed. For diabetic ketoacidosis: Regular insulin (Humulin R) 0.1 U/kg IV bolus, followed by 0.05-0.1 U/kg/hour as a constant rate infusion (CRI). Monitor blood glucose every 1-2 hours and adjust infusion rate. Fluid therapy: 0.9% sodium chloride or lactated Ringer's solution at 60-100 mL/kg/day IV, with potassium chloride supplementation (20-30 mEq/L) if hypokalemia is present. For urinary tract infections: Amoxicillin-clavulanate (Clavamox) 12.5-25 mg/kg PO every 8 hours for 10-14 days. For nausea or vomiting: Maropitant (Cerenia) 1 mg/kg SC once daily or 2 mg/kg PO once daily. For gastric protection: Famotidine 0.5-1 mg/kg PO/IV every 12-24 hours. For hepatic lipidosis support: S-adenosylmethionine (SAMe) 20 mg/kg PO once daily. For monitoring: Blood glucose curves should be performed every 1-2 weeks. Fructosamine should be measured every 2-4 weeks. Insulin doses should be adjusted based on the lowest blood glucose value in the curve. Always have dextrose (50% solution) available for emergency treatment of hypoglycemia (1-2 mL/kg IV diluted 1:1 with saline).

Evidence-based literature on gestational diabetes mellitus in dogs and cats is limited, but several key studies and reviews provide guidance. A landmark study by Fall et al. (2007) evaluated the prevalence of diabetes mellitus in dogs and found that a small percentage of cases were associated with pregnancy. Another study by Hess (2008) reviewed the management of diabetes in pregnant bitches, emphasizing the importance of insulin therapy and monitoring. In cats, a case report by Lederer et al. (2009) described successful management of GDM with glargine insulin. A retrospective study by Poppenga and Tvedten (2010) highlighted the risk factors and outcomes of GDM in dogs, noting that early diagnosis and treatment improved fetal survival. The American College of Veterinary Internal Medicine (ACVIM) consensus statement on diabetes mellitus in dogs and cats (2018) provides guidelines for diagnosis and management, including pregnancy. The European Society of Veterinary Endocrinology (ESVE) has also published recommendations. A study by Gilor et al. (2013) investigated the use of fructosamine for monitoring glycemic control in dogs and cats, supporting its use in GDM. Regarding fetal monitoring, a study by Zone et al. (1995) established reference ranges for fetal heart rate in dogs, which are used to assess fetal distress. A more recent study by Smith (2015) evaluated the use of ultrasonography in monitoring pregnancies complicated by diabetes. Overall, the evidence suggests that GDM is a rare but manageable condition, and that a combination of dietary modification, insulin therapy, and close monitoring can lead to successful outcomes. However, large-scale prospective studies are needed to establish standardized protocols.