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PubMed1980

Zinc deficiency, chronic starvation, and hypothalamic-pituitary-thyroid function.

Male Sprague-Dawley rats were fed a zinc-deficient diet to study its effects on the hypothalamic-pituitary-thyroid axis. As zinc-deficient animals fail to gain weight, they were compared to pair-fed growth restricted animals as well as ad libitum fed controls. The growth velocity curves were superimposable for the zinc-deficient animals and the pair-fed controls; both were markedly reduced compared to the ad libitum controls. Both the zinc-deficient and the pair-fed controls had lower triiodothyronine (T3) and thyroxine levels compared to the ad libitum controls. In addition T3 values were lower in the zinc-deficient animals compared to the pair-fed controls (P < 0.05). Hypothalamic thyrotrophin-releasing hormone content was decreased in the zinc-deficient rats (162 +/- 32 pg/ml) compared to the ad libitum controls (305 +/- 102; P < 0.01). The 125I thyroidal uptakes were not significantly different between the zinc-deficient and the pair-fed controls. Zinc deficiency lowers T3 more than comparable caloric restriction; this suggests that zinc deficiency may impair extrathyroidal production of T3.

Animals↗

PubMed1988

Role and management of exercise in diabetes mellitus.

As more is understood about the physiology of exercise, in both normal and diabetic subjects, its role in the treatment of diabetes is becoming better defined. Whereas people with diabetes may derive many benefits from regular physical exercise, there are also several hazards that make exercise difficult to manage. In type I (insulin-dependent) diabetes, there are risks of hypoglycemia during or after exercise or of worsening metabolic control if insulin deficiency is present. Type II (non-insulin-dependent) diabetic patients treated with sulfonylureas are also at some increased risk of developing hypoglycemia during or after exercise, although this poses less of a problem than with insulin treatment. In individuals treated by diet alone, regulation of blood glucose during exercise is usually not a significant problem and exercise can be used as an adjunct to diet to achieve weight loss and improved insulin sensitivity. When obese type II diabetic patients are treated with very low calorie diets, adequate amounts of carbohydrate must be provided to ensure maintenance of normal muscle glycogen content, particularly if individuals wish to participate in high-intensity exercise that places a heavy workload on specific muscle groups. On the other hand, moderate-intensity exercise such as vigorous walking can be tolerated by individuals on very low calorie, carbohydrate-restricted diets after an appropriate period of adaptation. A number of strategies can be employed to avoid hypoglycemia in type I diabetic patients, and both type I and II diabetic patients should be examined carefully for long-term complications of their disease, which may be made worse by exercise. These considerations have led many diabetologists to consider exercise beneficial in the management of diabetes for some individuals but not recommended for everyone as a necessary part of diabetes treatment as in the past. The goals should be to teach patients to incorporate exercise into their daily lives if they wish and to develop strategies to avoid the complications of exercise. The rationale for the use of exercise as part of the treatment program in type II diabetes is much more clear than for type I diabetes; regular exercise may be prescribed as an adjunct to caloric restriction for weight reduction and as a means to improve insulin sensitivity in the obese insulin-resistant individual.

Diabetes Mellitus, Type 1↗

PubMed1988

Regulation of bile acid pool size and plasma lipid levels in the SHR/N-corpulent rat: influence of the level of caloric intake.

In the obese progeny of the SHR/N-cp strain of the rat the bile acid pool was at least twice as large as that in their lean littermates even when only 6 weeks old. The composition of the pool remained unchanged in the obese females, but in their male counterparts the proportion of cholic acid was significantly increased. Cholestyramine feeding reduced the pool size by 26% in the obese rats, but a similar effect also occurred in the lean animals. The obese rats consumed about 60% more food per day than their lean littermates. When obese females were pair-fed to the intake of their lean controls from 6 to 11 weeks of age, the bile acid pool remained significantly enlarged, although not to the same extent as in the obese rats fed ad lib. Plasma cholesterol levels were reduced but remained significantly higher than the levels in the lean animals. The marked hypertriglyceridemia exhibited by the obese rats fed ad libitum did not develop in their pair-fed counterparts. In contrast, there was a comparatively smaller reduction in plasma cholesterol and triglyceride levels in the obese rats fed cholestyramine. Hepatic steatosis persisted in the pair-fed animals as well as in those given cholestyramine. Restricting caloric intake significantly reduced the body weight gain of the obese rats but had little effect on the extent of their corpulence. These studies show that at least some of the characteristics of this congenic strain, including hypertriglyceridemia and hepatic and intestinal hypertrophy, are due mainly to excess dietary intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

The effects of overfeeding and dietary restriction on Sprague-Dawley rat survival and early pathology biomarkers of aging.

A significant correlation exists between average daily food consumption and 2-yr survival in control ad libitum (AL)-fed Sprague-Dawley (SD) rats. SD rats were fed Purina Rodent Chow 5002 or a modified chow, 5002-9, with lower protein, fat, metabolizable energy and increased fiber AL or by dietary restriction (DR) to 65% of the AL amount by measurement or time (6.5 hr). At 52 wk, food consumption and key pathology biomarkers correlated with 106-wk survival. The modified chow, 5002-9 fed AL, did not significantly improve survival. SD rats fed either diet AL consumed the greatest amount of feed and kcal/rat but consumed the same amount of feed per gram body weight as DR-fed rats. At 52 wk, AL rats fed either diet had the same brain weights as DR rats, but the AL-fed rats had greater body weight and body fat content and increased heart, lung, kidney, liver, adrenal, thyroid, and pituitary weights as well as an increased incidence and severity of degenerative and/or proliferative lesions in these organs. This study demonstrates that overfeeding best correlates with low 2-yr survival in SD rats and that simple DR by caloric restriction modifies key pathology biomarkers in the pituitary, mammary gland, kidney, and heart of SD rats at 52 wk that are predictive of 106-wk survival.

Aging↗

PubMed1988

Exercise and diabetes mellitus.

As more is understood about the physiology of exercise, both in normal and in diabetic subjects, its role in the treatment of diabetes is becoming better defined. Although persons with diabetes may derive many benefits from regular physical exercise, there also are a number of hazards that make exercise difficult to manage. In insulin-treated diabetics, there are risks of hypoglycemia during or after exercise or of worsening metabolic control if insulin deficiency is present. Type II diabetics being treated with sulfonylureas also are at some increased risk of developing hypoglycemia during or following exercise, although this is less of a problem than occurs with insulin treatment. In individuals treated by diet alone, regulation of blood glucose during exercise usually results in a decrease in glucose concentration toward normal but not to hypoglycemic levels and exercise can be used safely as an adjunct to diet to achieve weight loss and improved insulin sensitivity. When obese patients with type II diabetes are treated with very low calorie diets, adequate amounts of carbohydrate must be provided to ensure maintenance of normal muscle glycogen content, particularly if individuals wish to participate in high intensity exercise that places a heavy workload on specific muscle groups. On the other hand, moderate intensity exercise such as vigorous walking can be tolerated by individuals on very low calorie, carbohydrate-restricted diets after an appropriate period of adaptation. A number of strategies can be employed to avoid hypoglycemia in patients with insulin-treated diabetes and both type I and type II diabetic subjects should be examined carefully for long term complications of their disease, which may be worsened by exercise. These considerations have led many diabetologists to consider exercise to be beneficial in the management of diabetes for some individuals but not to be recommended for everyone as a "necessary" part of diabetic treatment as was thought in the past. Instead, the goals should be to teach patients to incorporate exercise into their daily lives if they wish and to develop strategies to avoid the complications of exercise. The rationale for the use of exercise as part of the treatment program in type II diabetes is much clearer and regular exercise may be prescribed as an adjunct to caloric restriction for weight reduction and as a means of improving insulin sensitivity in the obese, insulin-resistant individual.

Blood Glucose↗

PubMed1984

Cholesterol metabolism in the laying hen as influenced by dietary cholesterol, caloric intake, and genotype.

Three trials, each with 24 hens, were conducted to determine the effects of dietary cholesterol, caloric intake, and genotype on the synthesis, storage, and excretion of cholesterol in the laying hen. The two genotypes of birds used in this experiment had been divergently selected for high and low oxygen consumption and had been shown to differ significantly (P less than .01) in body weight gain and carcass lipid deposition from 0 to 4 weeks of age. The dietary treatment, administered for a 2-week period to birds in each genotype, consisted of two levels of dietary cholesterol (0 and 1% added) and two energy intakes (ad libitum and 75% ad libitum). The experimental design was a 2 X 2 X 2 factorial. One percent added cholesterol versus none supplemented produced a significant (P less than .01) decrease in available metabolizable energy and uptake of acetate into liver cholesterol while causing significant (P less than .01) increases in egg and liver cholesterol but not in plasma cholesterol. Restricting caloric intake, as compared to ad libitum feeding, resulted in significantly (P less than .01) decreased egg production and total amount of cholesterol excreted via the egg with significantly (P less than .05) increased plasma and liver cholesterol levels but no change in egg cholesterol concentration. Differences were significant (P less than .05) between the two genotypes in feed intake and hepatic cholesterol and lipid synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Nutritional regulation of the placental lactogen receptor in fetal liver: implications for fetal metabolism and growth.

We have recently identified and purified from fetal liver a distinct receptor that mediates the effects of placental lactogen (PL) on amino acid transport, glycogen synthesis, and somatomedin production in fetal tissues. At present, the factors that regulate the number and affinity of PL receptors in the fetus are unknown. Since maternal nutrition plays a critical role in fetal metabolism and growth, we have examined the role of nutrition in the regulation of the PL receptor in fetal lambs. Pregnant ewes at 123-126 days gestation were fed ad libitum (FED), fasted for 3 days (FASTED), or fasted for 3 days and then refed for an additional 3 days (REFED). The ewes were then killed, and the binding of [125I]ovine (o) PL to hepatic microsomes from the fetal lambs was examined. Maternal fasting caused a 60-75% reduction in the specific binding of oPL to fetal liver; the effect of fasting was reversed in part by refeeding [specific binding per mg protein: FED, 11.8 +/- 2.2% (n = 8); FASTED, 2.8 +/- 0.4% (n = 7); REFED, 7.2 +/- 2.6% (n = 3)]. The decrease in oPL binding resulted from an 80% reduction in the number of fetal oPL-binding sites (Scatchard analysis); there were no changes in the affinity of the oPL receptor (Kd, 0.6 nM), the subunit structure of the receptor, or the degree of occupancy of the receptor in vivo by endogenous fetal hormones. The specific bindings of GH (0.6%), PRL (0.3%), and insulin (35%) to fetal liver were not affected by maternal fasting, indicating that caloric restriction exerted a specific effect on oPL binding in the fetus. The number of fetal oPL-binding sites was positively correlated with the fetal liver glycogen content (r = 0.69; P less than 0.01) and the fetal plasma concentrations of glucose (r = 0.68; P less than 0.01) and insulin-like growth factor-I (r = 0.74; P less than 0.001), suggesting a role for the PL receptor in the regulation of fetal carbohydrate metabolism and growth. The number of fetal PL receptors was inversely correlated with the fetal plasma oPL concentration (r = 0.47; P less than 0.05). These studies demonstrate that fasting of the pregnant ewe reduces the number of PL receptors in ovine fetal liver. The reduction in fetal hepatic PL receptors may contribute to the mobilization and depletion of fetal liver glycogen stores and may play a role in the pathogenesis of the fetal growth retardation that accompanies maternal caloric deprivation.

Animals↗

PubMed1997

Effects of changes in calorie intake on intestinal nutrient uptake and transporter mRNA levels in aged mice.

In aged, chronically calorie-restricted (CR) mice, intestinal nutrient uptake is significantly higher than in same-age ad libitum controls. Can this chronic restriction-induced enhancement of uptake be reversed by ad libitum feeding? We addressed this question by switching 32-mo-old chronically CR mice to ad libitum feeding for 4 wk (CRAL). Intestinal transport rate and total intestinal absorptive capacity for D-sugars and several nonessential L-amino acids decreased significantly in CRAL mice. In contrast, switching CR mice to an ad libitum regimen for only 3 d had no effect on intestinal nutrient transport, indicating that the negative effects of ad libitum feeding require a duration longer than the 3-d lifetime of most enterocytes. Permeability of the intestinal mucosa to L-glucose was independent of the switches in diet. Levels of the brushborder glucose transporter SGLT1, brushborder fructose transporter GLUT5, and basolateral sugar transporter GLUT2 mRNA as determined by reverse transcriptase-polymerase chain reaction in 6-, 24-, and 32-mo-old mice were each apparently independent of caloric restriction and age. We conclude that the high rates of intestinal nutrient uptake exhibited by chronically CR mice can be reversed by ad libitum feeding of only 1 mo duration. These decreases in uptake were due mainly to specific decreases in transport per unit weight of intestine and not to nonspecific decreases in intestinal mass. Changes in rates of sugar uptake induced by chronic CR and age are apparently not accompanied by changes in steady-state levels of mRNA coding for those transporters.

Aging↗

PubMed1998

Depression in the quantity of intestinal secretory IgA and in the expression of the polymeric immunoglobulin receptor in caloric deficiency of the weanling mouse.

The objective of this investigation was to determine the influence of weanling caloric restriction on the expression of the polymeric immunoglobulin receptor (pIgR) in the liver and intestine and on the levels of IgA in the blood and intestinal secretions. Male C57BL/6J mice were allocated to a zero-time control group (19 days of age) or to groups fed for 14 days as follows: ad libitum intake of a complete purified diet (19% crude protein, 17 kJ/g gross energy) or restricted intake of a complete diet. Enzyme-linked immunosorbent assays revealed a low concentration of gut luminal immunoglobulin A (IgA) despite a normal concentration of serum IgA in the malnourished mice. The concentration and total quantity per organ of the pIgR were assessed in the liver and intestine by means of Western immunoblotting using an antiserum raised against the secretory component portion of rat pIgR. Malnourished animals exhibited low quantities of hepatic and intestinal pIgR relative to well-nourished controls (8% and 40% of control, respectively) and also exhibited a low concentration (soluble protein basis) of hepatic pIgR (39% of control). The concentration of biliary secretory component was also low in the malnourished animals (20% of well nourished). Despite the low quantity of hepatic pIgR, Western blotting revealed no change in the concentration of monomeric, dimeric, and polymeric forms of serum IgA in the malnourished group relative to well-nourished animals. Caloric deficiency in an experimental system that closely resembles human marasmus results in a decrease in the quantity of the pIgR that is sufficient to account for the low concentration of IgA in the mucous secretions of the intestine. Considered together with recent evidence pertaining to weanling protein deficiency, these results permit the conclusion that the pIgR is a focal point of the impact exerted by metabolically diverse forms of protein-energy malnutrition on mucosal humoral immunocompetence.

Animals↗

PubMed2006

A thin phenotype is protective for impaired glucose tolerance and related to low birth weight in mice.

BACKGROUND: Low birth weight is an independent risk factor for impaired glucose tolerance (IGT) and diabetes in adult life. This risk extends to both preterm and term infants, a particularly important finding given the increased survival of low-birth-weight infants with improvements in neonatal care. One potential strategy for prevention of low-birth-weight-associated glucose intolerance is postnatal nutritional modification and prevention of early postnatal weight gain. To determine the efficacy of this approach, we utilized our mouse model of low birth weight related to maternal undernutrition during the third week of pregnancy. METHODS: We studied three experimental groups of offspring mice: controls (C), undernutrition with low birth weight (UN) fed ad lib postnatally, and undernutrition with food restriction continued in postnatal life (UN-UN). Mean birth weight was significantly reduced in both groups of undernutrition offspring in utero (C: 1.86 +/- 0.03 vs. UN: 1.37 +/- 0.04 and UN-UN: 1.32 +/- 0.06, p <0.001). As expected, and in accord with human data, differences in weight between C and UN mice disappeared by week 2 of life, indicating catch-up growth in the UN group. RESULTS: Body weight was similar in all groups until 4 months of age, after which the UN-UN group had reduced body weight as compared with controls (p <0.05 at 6 months). Insulin tolerance test (1 U/kg), glucose tolerance test (2 g/kg) and glucose-stimulated insulin secretion test (3 g/kg) at 2 months of age were identical among C, UN, and UN-UN groups. By age 6 months, IGT had developed in the UN mice (p <0.05 vs. C). By contrast, UN offspring with caloric restriction postnatally (UN-UN) were protected from the development of glucose intolerance, with glucose levels identical to that of control mice. These differences appeared to be related to improved insulin sensitivity in the UN-UN mice as compared with UN mice, although data did not reach statistical significance. CONCLUSIONS: Our data suggest that alterations in early postnatal nutrition are associated with prevention of weight gain and the development of IGT in low-birth-weight mice.

Animals↗

PubMed1987

A comparison of constant feeding with bouts of fasting-refeeding at three levels of nutrition in the rat.

To investigate whether intermittent fasting alters subsequent utilization of ingested energy, we compared, in six groups of 450-g male Wistar rats, two modalities of food delivery: constant (CO) vs fasting for 3 days and refeeding for 7 days (F/RF). Both modalities were investigated at three planes of nutrition (100, 60 and 40 percent of ad libitum). The F/RF groups were offered, during the 7 days of refeeding, the same amount of food as the CO groups were offered in 10 days. With both 60 and 40 percent food restriction, there were no differences in body weight, body composition, or energy utilization between the F/RF and the CO groups after 4 (40 days) or 8 (80 days) cycles of fasting-refeeding. However, at both 40 and 80 days of study, lipoprotein lipase (LPL) activity was significantly higher in F/RF rats than in CO rats at all three planes of nutrition. Because 100 percent F/RF rats did not eat all food available during each refeeding period, a second experiment was conducted. Rats were fasted for 3 days then refed ad libitum until they reached the weights of 100 percent CO rats. The two groups did not differ in body weight, food intake, body composition or LPL activity after 4 (40 days) fasting-refeeding cycles. Thus, weight cycling produced by repeated bouts of fasting-refeeding did not result in increased efficiency of energy utilization. However, the combination of fasting-refeeding and overall caloric restriction produced greater LPL activity than constant food restriction. It has not been determined whether this elevated LPL activity would affect lipid accumulation upon ad-libitum refeeding.

Adipose Tissue↗

PubMed1990

Impact of energy intake and exercise on resting metabolic rate.

Resting metabolic rate is modulated by the amount of calories consumed in the diet relative to energy expenditure. Excessive consumption of energy appears to increase resting metabolic rate while fasting and very low calorie dieting causes resting metabolic rate to decrease. Since the metabolic rate at rest is the primary component of daily energy expenditure, its reduction with caloric restriction makes it difficult for obese individuals to lose weight and to maintain weight that is lost. Whether exercise has a carry-over effect on resting metabolic rate remains controversial, even though this question has been studied extensively during the last 90 years. Reasons for contradictory results include variations in control of prior diet and exercise patterns, inadequate exercise frequency, intensity and duration, and the possibility of response to exercise varying between individuals. Several lines of evidence suggest exercise may modulate resting metabolic rate. Bed rest in sedentary individuals leads to a reduction in resting metabolic rate. Similarly, in highly trained runners, cessation of daily exercise training lowers resting metabolic rate by about 7 to 10%. Resting metabolic rate is depressed in previously sedentary obese individuals on a very low calorie diet, but it quickly returns to the predieting level when exercise of sufficient frequency, intensity and duration is undertaken while dieting. These findings suggest caloric intake and daily exercise can modulate resting metabolic rate. Exercise of adequate intensity and duration may also enhance resting metabolic rate.

Basal Metabolism↗

PubMedDate not supplied

The early effects of dietary restriction on the pathogenesis of chronic renal disease in Sprague-Dawley rats at 12 months.

This study evaluated the effects of different diets and dietary regimens on the pathogenesis of chronic renal disease (CRD) in Sprague-Dawley rats at 52 wk and correlated these data with survival at 106 wk. A commercial diet (5002) was compared to a modified diet (5002-9) with less protein, fat, and energy and more fiber. Both diets were fed by ad libitum (AL) or dietary restriction (DR) regimens. The glomerular area (GA), glomerular sclerotic index (GSI), tubulo-interstitial index (TII), and tubular labeling index (tubular LI) were measured. The 5002-9 diet fed AL did not decrease the severity of CRD or increase survival, nor did the 5002 diet fed 6.5 hr/day. Both diets fed by DR did improve CRD and survival. Both AL groups had higher indices, and the 5002 AL males had the highest GA and GSI. These data indicate that the initial events in CRD occur as glomerular hypertrophy. Because the TII and tubular LI were only increased with advanced CRD, tubulo-interstitial damage did not occur until the glomerular changes were established. The 52-wk glomerular indices correlated with survival at 106 wk. Increased GA at 52 wk predicted low survival rates at 106 wk. These findings support a hypothesis that glomerular sclerosis and tubulo-interstitial damage occur secondary to early initial glomerular hypertrophy that is mitigated by caloric restriction.

Animals↗

PubMed1999

Caloric intake and aging: mechanisms in rodents and a study in nonhuman primates.

Caloric restriction (CR) increases maximum life span in rodents while attenuating the development of age-associated pathological and biological changes. Although nearly all of the rodent studies have initiated CR early in life (1-3 months of age), CR, when started at 12 months of age, also extends maximum life span in mice. Two main questions face investigators of CR. One concerns the mechanisms by which CR retards aging and diseases in rodents. There is evidence that CR may act, at least in part, by reducing oxidative stress. A CR-induced decrease in oxidative stress appears to be most profound in post-mitotic tissues and may derive from lower mitochondrial production of free radicals. The second issue is whether CR will exert similar effects in primates. Studies on CR in rhesus monkeys (maximum life span approximately 40 years) support the notion of human translatability. We describe the University of Wisconsin Study of rhesus monkeys subjected to a 30% reduction of caloric intake starting at either 1989 or 1994 when they were approximately 10 years old. The data from our study and from other trials suggest that CR can be safely carried out in monkeys and that certain physiological effects of CR that occur in rodents (e.g., decreased blood glucose and insulin levels, improved insulin sensitivity, and lowering of body temperature) also occur in monkeys. Whether oxidative stress in monkeys is reduced by CR will be known by the year 2000, while effects on longevity and diseases should be clearly seen by, appropriately, 2020.

Aging↗

PubMed1977

Long-term tryptophan restriction and aging in the rat.

Growth-retarded rats fed a tryptophan deficient diet at 21 days for periods of 6-22 months were shown to reach normal body weight when subsequently fed Purina Rat Chow. They demonstrated an increased ability over similar aged controls to recover from hypothermia induced by 3-minute whole-body ice water immersion, were able to bear litters at 17--28 months of age, showed a delay in the age of onset of visible tumors, and indicated an increase in their average lifespan at late ages. Animals fed on this diet from 3 months of age revealed a similar ability to reproduce at advanced ages, but not as marked as those placed on the diet earlier. The average lifespan (in months +/- the standard error of the mean) of the rats recovering from the long-term tryptophan-deficient diets was 36.31 +/- 2.26 while the control rats survived an average of 30.5 +/- 1.90 months. The last of 8 rats surviving the period of tryptophan-deficiency died at 45.50 months (1387 days) while the last of 14 control rats died at 41.75 months (1266 days). It is hypothesized that some kind of subtle mechanism exerts its influence on the rats during the period of tryptophan deficiency which caused an accelerated morbidity and mortality as they approached senescence approximately 1 to 2 years after refeeding. This is parallel to the situation with immature animals subjected to long-term caloric restriction and then fed on normal diets.

Aging↗

PubMed1986

Exercise adaptation responses for gastric inhibitory polypeptide (GIP) and insulin in obese children. Possible extra-pancreatic effects.

Thirteen obese children and matched controls were fed a mixed meal, and responses were evaluated at fixed intervals for glucose, insulin, and gastric inhibitory polypeptide (GIP). The obese children were evaluated before and within 48 h after completion of a 5-mo exercise training program (ETP). The ETP included three aerobic exercise sessions per week and modest diet restrictions. Caloric expenditure was increased by approximately 300 kcal/exercise session. Weight gain was minimal over the 5 mo. An unexpected increase in GIP response and improved insulin tolerance were recorded for the obese children post-ETP. GIP values were higher (P less than 0.05) at 30 and 60 min and led to a highly significant elevation (P less than 0.01) of the integrated GIP response for post-ETP obese versus both pre-ETP and normal-weight controls. Insulin values were lower (P less than 0.05) at 30 and 60 min and led to a lower integrated insulin response (P less than 0.0585) for post-ETP obese children. However, the obese children continued to secrete more insulin (P less than 0.05) than normal-weight controls. Glucose tolerance, similar for pre-ETP obese subjects and controls, did not change in post-ETP children. Exercise-induced improvement in glucose utilization in these obese children was associated with an increase in GIP secretion. This contrasts with reports that calorie restriction will improve glucose utilization with decreased insulin and GIP secretion. The study demonstrates a previously unreported uncoupling of GIP and insulin secretion and suggests shifts in peripheral tissue sensitivity to insulin-induced glucose uptake. These shifts may, in part, be influenced by GIP.

Adolescent↗

PubMed1997

Hind III polymorphism of the lipoprotein lipase gene and plasma lipid response to low calorie diet.

OBJECTIVE: To assess the effects of a low calorie diet on plasma lipids according to the Hind III polymorphism of the lipoprotein lipase (LPL) gene in overweight patients. DESIGN: Diet intervention study (25% restriction in energy intake during 2.5 months) in relation to genetic factors. SUBJECTS: 115 unrelated patients (77 women and 38 men) recruited on the basis of 120% of ideal body weight. MEASUREMENTS: Body weight, body mass index, blood lipids and lipoproteins, at entry and after 2.5 months, determination of LPL Hind III genotypes. RESULTS: On spontaneous diet, lipid and lipoproteins differed significantly between Hind III genotypes. Homozygous subjects for the presence of the Hind III cutting site, H2H2, had significantly higher plasma and VLDL triglyceride and apolipoprotein B concentrations than subjects carrying H1 allele. H2H2 subjects reduced their VLDL-triglyceride and apolipoprotein B concentrations more than H1 carriers, in such a way that differences in lipid levels according to genotypes were no more significant after diet. The magnitude of the decrease in triglycerides was positively correlated with the initial concentration but, among hypertriglyceridemic subjects, H2H2 still had the largest decrease in plasma and VLDL-triglycerides. CONCLUSION: The genetic variation at the LPL gene locus affects the response of serum lipid levels to caloric restriction. Overweight subjects with the H2H2 genotype of the LPL Hind III polymorphism are predisposed to hypertriglyceridemia but they are good responders to diet in terms of lipid levels.

Adult↗

PubMed2003

Genotype and age influence the effect of caloric intake on mortality in mice.

Long-term caloric restriction (CR) has been repeatedly shown to increase life span and delay the onset of age-associated pathologies in laboratory mice and rats. The purpose of the current study was to determine whether the CR-associated increase in life span occurs in all strains of mice or only in some genotypes and whether the effects of CR and ad libitum (AL) feeding on mortality accrue gradually or are rapidly inducible and reversible. In one experiment, groups of male C57BL/6, DBA/2, and B6D2F1 mice were fed AL or CR (60% of AL) diets beginning at 4 months of age until death. In the companion study, separate groups of mice were maintained chronically on AL or CR regimens until 7, 17, or 22-24 months of age, after which, half of each AL and CR group was switched to the opposite regimen for 11 wk. This procedure yielded four experimental groups for each genotype, namely AL-->AL, AL-->CR, CR-->CR, and CR-->AL, designated according to long-term and short-term caloric regimen, respectively. Long-term CR resulted in increased median and maximum life span in C57BL/6 and B6D2F1 mice but failed to affect either parameter in the DBA/2 mice. The shift from AL-->CR increased mortality in 17- and 24-month-old mice, whereas the shift from CR-->AL did not significantly affect mortality of any age group. Such increased risk of mortality following implementation of CR at older ages was evident in all three strains but was most dramatic in DBA/2 mice. Results of this study indicate that CR does not have beneficial effects in all strains of mice, and it increases rather than decreases mortality if initiated in advanced age.

Aging↗