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Effects of short-term caloric restriction on lactational performance of well-nourished women.

Milk volume and composition, nutrient intake and plasma prolactin levels of 22 well-nourished lactating women were measured during a 3-week period; an experimental group (E, n = 14) reduced energy intake by 19 to 53% (mean 32%) during week 2 while controls (C, n = 8) maintained normal intake. Mean maternal energy intakes (kcal/day) were: (E) 2316 (wk 1), 1591 (wk 2); (C) 2037, 2121. Mean infant milk intakes (g/day) during these weeks were: (E) 736, 718, 684; (C) 714, 671, 702. Milk intake was not reduced among infants of mothers whose energy intakes were at least 1500 kcal/day during week 2. In group E prolactin levels tended to increase during week 2. Milk composition did not change significantly. Lower energy intakes than those currently recommended appear compatible with successful lactation and gradual maternal weight loss, but longer-term studies are needed to determine a lower limit for safe intakes.

Adult↗

Effects of excessive caloric intake and caloric restriction on body weight and energy expenditure at rest and light exercise.

The individual response to overeating and semistarvation on energy expenditure at rest and light work before and after a test meal was investigated. This response was related to the change in dry body weight, measured as weight (W) minus total body water (TBW). Experiments were performed on 9 non-obese subjects: (a) with a normal habitual energy intake; (b) (overfeeding) with an extra energy intake of 12 MJ per day for two weeks; and (c) (semistarving) with an energy intake of only 2.1 MJ per day for 2 weeks. Measurements of VO2, VCO2, W and TBW were obtained at the end of each of the three periods. It was found that the perturbation in energy intake from normal to 20-25 MJ per day increased the energy expenditure. The magnitude of this increase was highly individual and inversely related to the change in dry body weight. Energy expenditure, measured under the four standardized conditions, after 2 weeks of starvation was lower than that obtained after the preceding overeating period. This decrease was also roughly inversely related to the change in dry body weight. The results support the idea that part of the regulation of body energy content takes place by way of a change in the efficiency of energy utilization and that the response to a perturbed energy intake varies considerably between subjects.

Adult↗

Chondrosarcoma growth: influence of diabetes, caloric restriction, and insulin treatment.

Diabetes and malnutrition result in decreased somatomedin production and cartilage growth in rats. The growth and metabolism of the Swarm rat chondrosarcoma are dramatically affected by somatomedins. Data presented here show that streptozotocin diabetes and diet restriction inhibit in vivo chondrosarcoma growth. Tumors grown in diabetic rats were significantly smaller than tumors grown in diet-restricted rats showing the same changes in body weight. Insulin treatment increased the rate of tumor growth in diabetic rats. Tumors grown in rigidly controlled diabetic rats were as large as tumors grown in nondiabetic controls. Diet restriction and diabetes reduced the capacity of the serum of the rat to stimulate alpha-amino[14C]isobutyrate uptake and [3H]uridine incorporation into RNA in chondrosarcoma pieces grown in nondiabetic rats. This somatomedin activity of the serum was restored by treating diabetic rats with insulin. There was a significant correlation between the in vitro stimulatory effect of a particular serum pool on chondrosarcoma metabolism and in vivo chondrosarcoma growth in the animals from whom the serum was obtained. These studies demonstrate that the in vivo growth of malignant chondrocytes is similar to that of normal chondrocytes with respect to the role of nutrition and insulin.

Animals↗

Effects of variable caloric restriction on utilization of ingested energy in rats.

Body weight reductions were produced in five groups of male Wistar rats (325 g) by starvation or by variable degrees of underfeeding. The resulting body weights were maintained, by adjusting daily food intake, at constant levels for at least 18 days. We found that 1) energy conservation (i.e., a reduction in the amount of energy required for maintenance) developed in proportion to reduction in body weight, 2) energy conservation increased even while reduced body weights were maintained at constant levels, 3) reduction in the energy required for maintenance was largely due to reduced resting metabolic rate, 4) a maximal ability to conserve energy seemed to occur in severely food-restricted rats, and 5) the magnitude of energy conservation appeared to be proportional to the absolute reduction in body weight and was unrelated (in the long run) to rapidity of weight loss. This study confirms that precise mechanisms of energy conservation are set in motion by food restriction and attempts to identify some components of this adaptive response.

Adipose Tissue, Brown↗

Effect of small doses of iodine on thyroid function during caloric restriction in normal subjects.

It is well recognized that starvation and malnutrition are associated with a low-T3 syndrome in man. A similar condition has been observed after intake of a low carbohydrate hypocaloric diet. However, little is known about the influence of iodine on these conditions. Therefore, we evaluated the effect of iodine supplementation on thyroid function before and after a short-term intake of a low carbohydrate diet in normal subjects residing in an iodine-deficient area. The study was performed in 16 young euthyroid, nonobese volunteers (11 males, 5 females). The subjects were placed on a low carbohydrate (800 kcal) diet for 4 days. Eight subjects received 500 micrograms iodine (oral) daily beginning 4 weeks before diet. The control group (n = 8) received no iodine. After iodine supplementation, iodine excretion increased from 52 to 405 micrograms iodine/g of creatinine. Total T4 showed a slight but significant increase (104.2 nmol/l vs. 115.8 micrograms/dl; p < 0.001); fT4 was unchanged. The intake of the hypocaloric low carbohydrate diet resulted in a striking decrease in both total and free T3 and an increase of rT3 irrespective of iodine supplementation. T4 and fT4 were not affected in either group. During diet, iodine administration resulted in a decrease of basal TSH from 2.3 to 1.2 mU/l (p < 0.05), delta TSH from 10.3 to 4.5 mU/l (p < 0.01) and delta T3 (T3 180 min after TRH) from 0.7 to 0.3 nmol/l (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Structure and function changes in the endocrine pancreas of aging rats with reference to the modulating effects of exercise and caloric restriction.

The current study was conducted to determine if physical activity and/or weight control could influence the age-related decrease in beta cell insulin response noted in earlier studies. As such, virgin, male Sprague-Dawley rats were maintained in our facility for 1 yr on three differential experimental programs; in the first group, control rats lived under standard laboratory conditions; the second group of rats ran several miles a day in exercise wheels, and the third group was given a calorie-restricted diet designed to keep the rats weight-matched with the exercising rats. The results showed that the 12-mo-old sedentary control rats weighed an average of 800g. From the time these rats were 4 mo old, they were significantly hyperinsulinemic, with mean (+/- SEM) serum insulin levels of 55 +/- 6 microU/ml. Morphological studies on the pancreas of these rats at the end of the year revealed enlarged, multilobulated, fibrotic islets. After collagenase digestion, the most normal-appearing islets from the 12-mo-old controls were used for insulin secretion studies, these islets showed significantly reduced glucose-induced insulin release (0.83 microU insulin/min per volume islet) compared with islets from young rats (1.80 microU insulin/min per volume islet). In contrast, 12-mo-old exercised or calorie-restricted rats weighed approximately 500 g and did not show the changes in serum insulin levels or pancreas pathology exhibited by the sedentary control animals. However, islets from the calorie-restricted group functioned in vitro no better than islets from he sedentary control group. Islets from the exercised rats were somewhat improved in this regard. In summary, we believe exercise and weight control diminishes the animals' need for insulin-resulting in youthful-appearing islets after a year's time. However, these regimes do not appear able to correct the beta cell decline in function previously described.

Aging↗

Caloric restriction reverses hepatic insulin resistance in aging rats by decreasing visceral fat.

Hyperinsulinemia and increased visceral/abdominal fat (VF) are common features of human aging. To examine the relationships among VF, peripheral, and hepatic insulin sensitivity, we studied 4- and 18-mo-old male Sprague-Dawley rats (n = 42) fed ad libitum (4 AL and 18 AL) or moderately calorie restricted (18 CR) up to 18 mo of age. Total fat mass (FM) and VF were decreased in 18 CR to approximately one-third of that of 18 AL (P < 0.001), while lean body mass (LBM) was unchanged. Most important, 18 CR had more FM (65+/-6 vs. 45+/-6 g) but less VF (7.8+/-0.6 vs. 12.3+/-3.3 g) compared with 4 AL (P < 0.01 for both). Thus, the effects of variable VF on HIS could be assessed, independent of FM and age. Marked hepatic insulin resistance ensued with aging (18 AL) and CR restored hepatic insulin sensitivity to the levels of young rats, while peripheral insulin sensitivity remained unchanged (by insulin clamp of 18 mU/kg/min). In fact, the rates of insulin infusion required to maintain basal hepatic glucose production in the presence of pancreatic clamp were 0.75+/-0.10, 1.41+/-0.13, and 0.51+/-0.12 mU/kg . min, in 4 AL, 18 AL, and 18 CR, respectively (P < 0.01 between all groups), and in 18 CR rats infused with insulin at similar rates as in the 18 AL (1.4 mU/kg/min) hepatic glucose production was decreased by 32% (P < 0. 005). Furthermore, when 18 CR rats were fed AL for 14 d, VF rapidly and selectively increased and severe hepatic insulin resistance was induced. We propose that in this animal model the age-associated decrease in hepatic (rather than peripheral) insulin action is the major determinant of fasting hyperinsulinemia and that increased visceral adiposity plays the major role in inducing hepatic insulin resistance. Thus, interventions designed to prevent the accumulation of VF are likely to represent an effective mean to improve carbohydrate metabolism in aging.

Adipose Tissue↗