**1. Diet in patients with gestational diabetes**

#### **1.1. Introduction**

Gestational diabetes mellitus (GDM) is described as any degree of carbohydrate intolerance first recognized during pregnancy [1]. GDM affects 4–8% of pregnant women in developed countries [2]. GDM is associated with an increased risk of adverse maternal and fetal outcomes, hence providing good glycemic control to substantially improve outcome [3].

Alterations in the secretion of growth hormone and cortisol and increase in human placental lactogen and insulinase levels are the mechanisms of insulin resistance during pregnancy.

Additionally, increased estrogen and progesterone make a contribution to the impaired glucose tolerance. The increase in adipose tissue, less exercise, and increased caloric intake during pregnancy are also other contributors [4].

values in early pregnancy [10]. Basal hepatic glucose production is also similar to the 12–14th week of pregnancy. Postprandial glucose concentrations are significantly elevated, and the glucose peak is prolonged. Basal glucose levels decrease by 10–15 mg/dL (0.56–0.83 mmol/L), insulin levels increased by two fold, and peak of glucose is prolonged at the third trimester [11]. Increased glucose production is seen by the increase in maternal body weight; however, glucose production per kilogram body weight remains unchanged during

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Plasma triacylglycerol, fatty acid, cholesterol, and phospholipid levels are altered as a result of changes in hepatic and adipose metabolism [13]. Their levels decrease at the early weeks of pregnancy; however, these levels steadily increase during pregnancy. The increase in estrogen levels and insulin resistance are potential mechanisms of hypertriglyceridemia in pregnancy [14]. Placenta uses cholesterol for steroid synthesis and fatty acids for placental oxidation and membrane formation [15]. Hepatic lipoprotein lipase decreases postprandially; however, it increases during fasting, which increases production of fatty acids and ketones for the fetus to compensate low glucose supply [14]. GDM induces a state of dyslipidemia consistent with insulin resistance. During pregnancy, women with GDM do have higher serum triacylglycerol concentrations, but lower LDL-cholesterol concentrations decrease during pregnancy; however, total cholesterol, HDL cholesterol, and apolipoprotein concentrations

Diagnosing women with GDM is extremely significant for close follow-up of the fetus throughout gestation and to identify women with risk of type 2 diabetes occurrence [17]. The main target of the medical treatment in GDM is to provide a good glycemic control, particularly for postprandial concentrations [2]. Treatment of gestational diabetes reduces serious perinatal morbidity and may also improve the woman's health related [18]. Serious perinatal morbidity is decreased, and maternal health-related quality of life is improved by the treatment of GDM. Although glucose goals throughout gestation are very strict, hypoglycemia should be avoided. Preconceptional target for HbA1c is <6.5% to decrease congenital

American Diabetes Association recommendation for glucose concentration goals in women

Glucose concentration goals in pregnant women with pre-existing type 1 or type 2 diabetes, if

• Premeal, bedtime, and overnight glucose 60–99 mg/dL (3.3–5.4 mmol/L)

gestation [12].

are not changed [14, 16].

anomalies [19].

• A1C <6.0% [20]

with GDM:

**1.4. Management of Diabetes in pregnancy**

• Fasting ≤95 mg/dL (5.3 mmol/L) and either

• One-hour postprandial ≤140 mg/dL (7.8 mmol/L) or

• Two-hour postprandial ≤120 mg/dL (6.7 mmol/L)

it can be achieved without excessive hypoglycemia:

• Peak postprandial glucose 100–129 mg/dL (5.4–7.1 mmol/L)

## **1.2. Diagnosis**

Diabetes diagnosed during the first trimester of pregnancy should be described as type 2 diabetes mellitus. GDM is diabetes diagnosed after the first trimester of pregnancy that is not clearly either type 1 or type 2 DM [5].

There are two strategies in diagnosing of GDM [5].

"One step" approach:

A 2-h 75-g oral glucose tolerance test (OGTT) is performed at 24–28 weeks of gestation in women without an overt diabetes diagnosis. Glucose concentrations after fasting and 1 and 2 h after glucose administration <92 mg/dL (5.1 mmol/L), <180 mg/dL (10.0 mmol/L), and <153 mg/dL (8.5 mmol/L), respectively, were accepted as normal; if the glucose concentration is over than the normal at any point, the patient is diagnosed with GDM.

"Two-step" approach:

Step 1: Perform a 50-gr OGTT (nonfasting), measure plasma glucose at 1 h, at 24–28 weeks of gestation in women without an overt diabetes diagnosis. If the plasma glucose concentration is higher than 140 mg/dL (7.8 mmol/L) at 1 h after the load, proceed to a 100-gr OGTT.

Step 2: Perform a 100-g OGTT when the patient is fasting. If the glucose concentration is more than the normal at least two of the following four plasma glucose levels, the patient diagnosed with GDM.


Although one-way strategy was shown to be cost-effective [6] and may be the preferred approach, data comparing population-wide outcomes with two strategies are contradictory [7, 8]. Longer term outcome studies are currently on the way.

#### **1.3. Metabolic changes during pregnancy**

Women with GDM do not have an essential β-cell reserve to produce adequate insulin to overcome the insülin resistance of pregnancy, and all women with GDM have a degree of impaired function of β-cell [9]. Basal glucose and insulin levels are similar to nongravid values in early pregnancy [10]. Basal hepatic glucose production is also similar to the 12–14th week of pregnancy. Postprandial glucose concentrations are significantly elevated, and the glucose peak is prolonged. Basal glucose levels decrease by 10–15 mg/dL (0.56–0.83 mmol/L), insulin levels increased by two fold, and peak of glucose is prolonged at the third trimester [11]. Increased glucose production is seen by the increase in maternal body weight; however, glucose production per kilogram body weight remains unchanged during gestation [12].

Plasma triacylglycerol, fatty acid, cholesterol, and phospholipid levels are altered as a result of changes in hepatic and adipose metabolism [13]. Their levels decrease at the early weeks of pregnancy; however, these levels steadily increase during pregnancy. The increase in estrogen levels and insulin resistance are potential mechanisms of hypertriglyceridemia in pregnancy [14]. Placenta uses cholesterol for steroid synthesis and fatty acids for placental oxidation and membrane formation [15]. Hepatic lipoprotein lipase decreases postprandially; however, it increases during fasting, which increases production of fatty acids and ketones for the fetus to compensate low glucose supply [14]. GDM induces a state of dyslipidemia consistent with insulin resistance. During pregnancy, women with GDM do have higher serum triacylglycerol concentrations, but lower LDL-cholesterol concentrations decrease during pregnancy; however, total cholesterol, HDL cholesterol, and apolipoprotein concentrations are not changed [14, 16].

#### **1.4. Management of Diabetes in pregnancy**

Additionally, increased estrogen and progesterone make a contribution to the impaired glucose tolerance. The increase in adipose tissue, less exercise, and increased caloric intake during preg-

Diabetes diagnosed during the first trimester of pregnancy should be described as type 2 diabetes mellitus. GDM is diabetes diagnosed after the first trimester of pregnancy that is not

A 2-h 75-g oral glucose tolerance test (OGTT) is performed at 24–28 weeks of gestation in women without an overt diabetes diagnosis. Glucose concentrations after fasting and 1 and 2 h after glucose administration <92 mg/dL (5.1 mmol/L), <180 mg/dL (10.0 mmol/L), and <153 mg/dL (8.5 mmol/L), respectively, were accepted as normal; if the glucose concentration is over than the normal at any point, the patient is diagnosed with GDM.

Step 1: Perform a 50-gr OGTT (nonfasting), measure plasma glucose at 1 h, at 24–28 weeks of gestation in women without an overt diabetes diagnosis. If the plasma glucose concentration is higher than 140 mg/dL (7.8 mmol/L) at 1 h after the load, proceed to a 100-gr OGTT. Step 2: Perform a 100-g OGTT when the patient is fasting. If the glucose concentration is more than the normal at least two of the following four plasma glucose levels, the patient

Although one-way strategy was shown to be cost-effective [6] and may be the preferred approach, data comparing population-wide outcomes with two strategies are contradictory

**Carpenter/Coustan or National Diabetes Data Group (NDDG)**

Fasting 95 mg/dL (5.3 mmol/L) 105 mg/dL (5.8 mmol/L) h 180 mg/dL (10.0 mmol/L) 190 mg/dL (10.6 mmol/L) h 155 mg/dL (8.6 mmol/L) 165 mg/dL (9.2 mmol/L) h 140 mg/dL (7.8 mmol/L) 145 mg/dL (8.0 mmol/L)

Women with GDM do not have an essential β-cell reserve to produce adequate insulin to overcome the insülin resistance of pregnancy, and all women with GDM have a degree of impaired function of β-cell [9]. Basal glucose and insulin levels are similar to nongravid

[7, 8]. Longer term outcome studies are currently on the way.

**1.3. Metabolic changes during pregnancy**

nancy are also other contributors [4].

clearly either type 1 or type 2 DM [5].

There are two strategies in diagnosing of GDM [5].

**1.2. Diagnosis**

146 Diabetes Food Plan

"One step" approach:

"Two-step" approach:

diagnosed with GDM.

Diagnosing women with GDM is extremely significant for close follow-up of the fetus throughout gestation and to identify women with risk of type 2 diabetes occurrence [17]. The main target of the medical treatment in GDM is to provide a good glycemic control, particularly for postprandial concentrations [2]. Treatment of gestational diabetes reduces serious perinatal morbidity and may also improve the woman's health related [18]. Serious perinatal morbidity is decreased, and maternal health-related quality of life is improved by the treatment of GDM. Although glucose goals throughout gestation are very strict, hypoglycemia should be avoided. Preconceptional target for HbA1c is <6.5% to decrease congenital anomalies [19].

American Diabetes Association recommendation for glucose concentration goals in women with GDM:


Glucose concentration goals in pregnant women with pre-existing type 1 or type 2 diabetes, if it can be achieved without excessive hypoglycemia:


GDM patients should have at least four blood glucose measurement daily (fasting and 1 h after the first bite of each meal) to monitor hyperglycemia that is known to increase the risk of adverse maternal and fetal outcomes. One-hour postprandial glucose monitoring provides a better glycemic control and fewer cases of large-for-gestational age infants compared to fasting glucose monitoring [21]. Postprandial monitoring provides a better glycemic control and lower risk of preeclampsia [22, 23].

**1.6. Energy**

in **Table 2**.

Low (BMI < 19.8 kg/m<sup>2</sup>

Normal (19.8–26.0 kg/m<sup>2</sup>

High (>26.0–29.0 kg/m<sup>2</sup>

Obese (≥29.0 kg/m<sup>2</sup>

Most of the patients with GDM are obese, and additional weight increase during pregnancy leads to adverse pregnancy outcome and long-term risk for development of T2DM. The recommendation of minimal weight gain in obese GDM patients has not been confirmed yet.

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Although significant caloric restriction in obese GDM patients may cause ketosis, moderate caloric restriction (decrease by 30% of estimated energy requirements) in these patients may provide a good glycemic control without ketonemia and decrease maternal weight gain. The data regarding how such diets have impact on fetal outcomes are lacking [34].

Adequate energy intake is recommended for proper weight gain. Moderate energy and carbohydrate limitation are recommended, instead of weight loss, for overweight, and obese GDM patients. The primary goals of MNT for GDM are proper weight gain, normoglycemia, and absence of ketosis [34]. The requirement for energy does not rise in the first trimester of gestation. An additional 300 kcal/day is recommended to compensate the increase in maternal blood flow, breast, uterus, adipose tissue, placental growth, fetal growth, and amniotic fluids after the first trimester. Nevertheless, a safe pregnancy is possible with lower energy intake [36]. Quality nutritional intake is required. A number of calories should be calculated according to ideal body weight. The recommendations for daily calorie intake were shown

Calorie recommendations may provide normoglycemia in 75–80% of GDM [4]. Reduction in caloric intake by 30–33% would help blood glucose management without increasing ketosis risk in obese women with GDM. Nevertheless, the caloric intake should not be less than 1600–1800 kcal/ day. In cases of calorie reduction, urine should be monitored for ketones.

The recommended overall dietary ratio: Carbohydrates: 40–50%, protein: 20–25%, and fat: 30–35%. Although restriction of carbohydrate intake to 40–45% of daily energy decreases post-

) 28–40 ~ 1.0 (0.5 kg/wk)

) 25–35 1.0 (0.4 kg/wk)

) 15–25 0.66 (0.3 kg/wk)

) ≥ 15 Not specified

**Table 1.** Recommendations for weight gain and rate of weight gain during pregnancy [35].

**Total weight gain (lb) Rate of weight gain in the second and** 

**third trimesters (lb/wk)**

Weight gain in pregnancy should represent pregestational weight [9].

Catabolic metabolism and malnutrition of fetus must be prevented.

**Prepregnancy BMI Mothers of singletons**

prandial glucose, the ratio of carbohydrates should not be lower than 40% [37].

Recommendations for weight gain during pregnancy were shown in **Table 1**.

GDM is associated with higher macrosomia risk and birth complications and an increased risk of maternal type 2 diabetes postpartum [3]. Diet, exercise, and lifestyle changes may decrease the risk of GDM [24, 25]. Lifestyle modification alone is sufficient in most of the patients to control GDM [26, 27]. However, early initiation of pharmacologic therapy might be needed when lifestyle modifications are insufficient for glycemic control.

Insulin is the recommended first-line agent in the treatment of GDM. Although randomized controlled trials demonstrated the efficacy and short-term safety of metformin [28, 29] and glyburide [30], long-term safety trials are still lacking for any oral drugs [31].
