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Biomedical subjects

L V Campbell

Publications and source records attributed to L V Campbell.

At least 19 recordsLinked to original sources
PubMed1997

Carbohydrate intake and short-term regulation of leptin in humans.

The response of serum leptin to short (4 days) and prolonged (28 days) energy restriction (50% reduction in energy intake) was determined in 18 (9 male, 9 female) moderately obese humans (body mass index 32.0 +/- 0.6 kg/m2 mean +/- SEM), 9 of whom had mild non-insulin-dependent diabetes mellitus (NIDDM). Body composition was assessed before and at the end of the energy restriction using DEXA. The subjects lost a measured 2.6 +/- 0.4 kg of body fat after 28 days and an estimated 0.3 kg at 4 days. Serum leptin fell to 64 +/- 3% of baseline levels at day 4 and further to 46 +/- 4% at day 28. In a multiple correlation analysis, the change in leptin concentration at day 4 was significantly related to the change in dietary carbohydrate intake (partial r = 0.68, p < 0.005) but not to changes in fat (r = 0.12) or protein (r = 0.02) intakes. There was a 1:1 relationship between the changes in leptin and dietary carbohydrate (regression slope = 1.0 +/- 0.3). Gender, or the presence of NIDDM had no effects on these responses. This pronounced fall in serum leptin in association with reduced carbohydrate intake before substantial loss of body fat suggests a role for leptin in defending the body's carbohydrate stores and implicates leptin in the satiating effects of carbohydrate. Dietary or other interventions which maintain leptin levels during weight reduction may lead to improvements in weight loss.

Analysis of Variance↗
PubMed1997

Independent genetic factors determine the amount and distribution of fat in women after the menopause.

Central adiposity is a strong predictor of cardiovascular disease in women. We studied postmenopausal twins to explore the strength and the relationship between genetic influences on body fat and its distribution in a group where cardiovascular disease is the major cause of mortality. Healthy twin women were recruited from a national media campaign. One hundred nineteen monozygotic (MZ) and 97 dizygotic twin pairs were studied (mean +/- SE age 60 +/- 0.3 yr; 10 +/- 0.4 yr post menopausal). Total and central body fat were measured by dual-energy x-ray absorptiometry. Intrapair resemblance was significantly greater in MZ pairs for total fat (MZ vs. dizygotic, r = 0.70 +/- 0.05 vs. r = 0.46 +/- 0.08, P = 0.005) and central fat (r = 0.62 +/- 0.06 vs. r = 0.35 +/- 0.09, P = 0.005), suggesting a strong genetic influence on these traits. Model-fitting analysis indicated that genetic factors contribute up to 60% of total population variance in both total and central body fat. The heritability of central fat remained, after adjustment for the heritability of total fat, suggesting an independent genetic influence on fat distribution. These results were unchanged after adjusting for the effects of estrogen replacement and smoking. In conclusion, total adiposity and central abdominal fat mass in normal postmenopausal women are under strong genetic influence. The data suggest that some of the genes responsible for central adiposity and its metabolic sequelae will be different from those responsible for total adiposity.

Adipose Tissue↗
PubMed1996

Abdominal fat and insulin resistance in normal and overweight women: Direct measurements reveal a strong relationship in subjects at both low and high risk of NIDDM.

Insulin resistance appears to be central to obesity, NIDDM, hyperlipidemia, and cardiovascular disease. While obese women with abdominal (android) fat distribution are more insulin resistant than those with peripheral (gynecoid) obesity, in nonobese women, the relationship between abdominal fat and insulin resistance is unknown. By measuring regional adiposity with dual-energy X-ray absorptiometry and insulin sensitivity by euglycemic-hyperinsulinemic clamp in 22 healthy women, with a mean +/- SE body BMI of 26.7 +/- 0.9 kg/m2 and differing risk factors for NIDDM, we found a strong negative relationship between central abdominal (intra-abdominal plus abdominal subcutaneous) fat and whole-body insulin sensitivity (r = -0.89, P < 0.0001) and nonoxidative glucose disposal (r = -0.77, P < 0.001), independent of total adiposity, family history of NIDDM, and past gestational diabetes. There was a large variation in insulin sensitivity, with a similar variation in central fat, even in those whose BMI was <25 kg/m2. Abdominal fat had a significantly stronger relationship with insulin sensitivity than peripheral nonabdominal fat (r2 = 0.79 vs. 0.44), and higher levels were associated with increased fasting nonesterified fatty acids, lipid oxidation, and hepatic glucose output. Because 79% of the variance in insulin sensitivity in this heterogeneous population was accounted for by central fat, abdominal adiposity appears to be a strong marker and may be a major determinant of insulin resistance in women.

Abdomen↗
PubMed1996

Glycemic responses to exercise in IDDM after simple and complex carbohydrate supplementation.

OBJECTIVE: Subjects with IDDM should take carbohydrate before exercise to avoid hypoglycemia. However, there is little information on the glycemic effect of recommended supplementation. This study is aimed to determine the glycemic effects of oral glucose or bread (30 g carbohydrate) before 45 min of moderate exercise. RESEARCH DESIGN AND METHODS: Nine subjects with uncomplicated IDDM did 45 min of bicycle ergometer exercise at 60% VO2max in the morning before insulin injection on three occasions: 1) with no carbohydrate supplement, 2) with 30 g glucose in water at -5 min, and 3) with 30 g carbohydrate as white bread with water at -20 min. The glycemic responses were determined. The glycemic responses to glucose and bread were also determined without exercise in six subjects. RESULTS: Without carbohydrate, exercise caused a small fall (-1.2 +/- 0.6 mmol/l, mean +/- SE) in plasma glucose (PG). With either glucose or bread, PG rose (the change in plasma glucose relative to basal [delta PG] = 5.1 +/- 0.8 and 2.6 +/- 0.8, respectively). The rise was greater (P < 0.01) without exercise (delta PG = 6.9 +/- 0.7 and 4.5 +/- 0.7, respectively). During exercise, glucose increased PG levels more than bread increased glucose levels P < 0.05). CONCLUSIONS: Before morning insulin injection, the fall in PG during moderate exercise in IDDM subjects is generally small or absent. The glycemic effects of complex carbohydrate are slightly less than glucose before exercise. Under these circumstances, the usually recommended amount of carbohydrate tends to cause an unwanted elevation of PG; thus, IDDM subjects should anticipate reducing or even omitting carbohydrate supplementation after monitoring their individual glycemic response.

Adolescent↗
PubMed1996

Genetic influences on central abdominal fat: a twin study.

INTRODUCTION: Recent studies of regional fat distribution have focused on the clinical importance of central abdominal obesity. Central adiposity is strongly related to insulin resistance, non-insulin dependent diabetes mellitus (NIDDM), dyslipidaemia and cardiovascular disease. While significant genetic influences on body mass index (BMI), total body and subcutaneous fat have been demonstrated, the inheritance of central abdominal obesity, has not been studied. OBJECTIVE: To assess genetic effects on regional fat distribution and associated metabolic parameters. DESIGN AND SUBJECTS: We directly measured total body, central abdominal (C-abd) and non-abdominal fat using dual energy X-ray absorptiometry in 50 monozygotic (MZ) and 36 dizygotic (DZ) female twins, of age (mean +/- SD), 44 +/- 12 and 47 +/- 14 y; BMI 24 +/- 5 and 24 +/- 3 kg/m2; C-abd fat 33 +/- 9 and 32 +/- 9%, respectively. Total variance in all parameters was independent of zygosity and genetic analyses of regional adiposity were performed before and after adjusting for age and percentage total body fat. RESULTS: A genetic influence was observed on the population variance in total fat, C-abd fat (C-abd fat rMZ = 0.66 vs rDZ = 0.20, p = 0.03) and non abdominal fat. After adjusting C-abd fat for age and total body fat there was a independent genetic influence on C-abd fat accounting for approximately 70% of the population variance (rMZ = 0.61 vs rDZ = 0.40, p = 0.001). CONCLUSION: The majority of inter-subject variance in central abdominal fat in non-obese individuals is due to genetic factors. The inheritance of abdominal obesity, with its associated metabolic consequences, may contribute to the familial aggregation of insulin resistance, diabetes and cardiovascular disease.

Abdomen↗
PubMed1995

Importance of early insulin levels on prandial glycaemic responses and thermogenesis in non-insulin-dependent diabetes mellitus.

To examine the effect of different profiles of insulin administration on glycaemia and thermogenesis, we studied 10 subjects with mild non-insulin-dependent diabetes mellitus on four occasions after a standard mixed meal: (1) with no supplementary insulin (control), (2) with intravenous insulin (1.8U over 15 min = short), (3) as for short but extended over 30 min to simulate the normal initial rise in portal vein insulin levels (medium), (4) as for medium with additional insulin to normalize the profile from 30-60 min (3.6U over 60 min, long). All studies in which supplemental insulin was administered lowered the integrated glucose response above baseline versus the control study (short 76%, medium 71%, and long 56% of control, p = 0.003). The insulin infusions also increased the non-protein respiratory quotient in the first hour following the meal (0.82 +/- 0.01 (control) vs 0.87 +/- 0.01 (short), 0.86 +/- 0.01 (medium) and 0.87 +/- 0.01 (long), p = 0.003) and augmented thermogenesis (7.6 +/- 1.5 (control) vs 10.5 +/- 2.9 (short), 13.0 +/- 1.9 (medium) and 13.2 +/- 2.8% (long), p = 0.02). Total integrated insulin area above baseline was significantly greater in the long study (short 121, medium 111 vs long 179% of control, p = 0.02). Thus the greatest glycaemic benefit in relation to insulinaemia was obtained with the two shorter insulin infusions (short and medium). In conclusion, this study confirms the role of early prandial insulin secretion (or delivery) in limiting prandial glycaemia in NIDDM and increasing thermogenesis and highlights the pivotal role of the timing of elevation of insulin levels in modulating hyperglycaemia and hyperinsulinaemia.

Aged↗
PubMed1994

The high-monounsaturated fat diet as a practical alternative for NIDDM.

OBJECTIVE: To examine the dietary preferences of and metabolic effects in patients with non-insulin-dependent diabetes mellitus (NIDDM) of a home-prepared high-monounsaturated fat (HM) diet compared with the recommended high-carbohydrate (CHO) diet. RESEARCH DESIGN AND METHODS: Ten men with mild NIDDM prepared HM and high-CHO diets at home alternately and in random order for 2 weeks each with a minimum 1-week washout. Before and after each diet, 24-h urine glucose, fasting lipids, fructosamine, and 6-h profiles of glucose, insulin, and triglycerides were measured. Dietary preferences were assessed by questionnaire. RESULTS: In the HM diet, patients consumed 40% of energy intake as CHO and 38% as fat (21% monounsaturated) compared with 52 and 24%, respectively, in the high-CHO diet, with equal dietary fiber content. Body weight and total energy intake were similar in both. The HM diet resulted in significantly lower 24-h urinary glucose excretion, fasting triglyceride, and mean profile glucose levels. The fructosamine levels, the fasting total, low-density lipoprotein, and high-density lipoprotein cholesterol, and the prandial triglyceride concentrations did not differ significantly as a result of the diets. The two diets did not differ in ratings for overall acceptance, taste, cost, ease of preparation, variety, or satiety. CONCLUSIONS: Prepared at home, the HM diet was, in the short-term, metabolically better in some aspects than the currently recommended diet for NIDDM. It also provided a palatable alternative.

Adult↗
PubMed1993

The relation between insulin sensitivity and the fatty-acid composition of skeletal-muscle phospholipids.

BACKGROUND: Insulin resistance and hyperinsulinemia are features of obesity, non-insulin-dependent diabetes mellitus, and other disorders. Skeletal muscle is a major site of insulin action, and insulin sensitivity may be related to the fatty-acid composition of the phospholipids within the muscle membranes involved in the action of insulin. METHODS: We determined the relation between the fatty-acid composition of skeletal-muscle phospholipids and insulin sensitivity in two groups of subjects. In one study, we obtained samples of the rectus abdominis muscle from 27 patients undergoing coronary artery surgery; fasting serum insulin levels provided an index of insulin sensitivity. In the second study, a biopsy of the vastus lateralis muscle was performed in 13 normal men, and insulin sensitivity was assessed by euglycemic-clamp studies. RESULTS: In the patients undergoing surgery, the fasting serum insulin concentration (a measure of insulin resistance) was negatively correlated with the percentage of individual long-chain polyunsaturated fatty acids in the phospholipid fraction of muscle, particularly arachidonic acid (r = -0.63, P < 0.001); the total percentage of C20-22 polyunsaturated fatty acids (r = -0.68, P < 0.001); the average degree of fatty-acid unsaturation (r = -0.61, P < 0.001); and the ratio of the percentage of C20:4 n-6 fatty acids to the percentage of C20:3 n-6 fatty acids (r = -0.55, P < 0.01), an index of fatty-acid desaturase activity. In the normal men, insulin sensitivity was positively correlated with the percentage of arachidonic acid in muscle (r = 0.76, P < 0.01), the total percentage of C20-22 polyunsaturated fatty acids (r = 0.76, P < 0.01), the average degree of fatty-acid unsaturation (r = 0.62, P < 0.05), and the ratio of C20:4 n-6 to C20:3 n-6 (rho = 0.76, P = 0.007). CONCLUSIONS: Decreased insulin sensitivity is associated with decreased concentrations of polyunsaturated fatty acids in skeletal-muscle phospholipids, raising the possibility that changes in the fatty-acid composition of muscles modulate the action of insulin.

Aged↗
PubMed1993

The platelet angiotensin II receptor in type I diabetes: studies in patients with and without nephropathy.

Experimental studies demonstrate impaired regulation of the mesangial angiotensin II (AII) receptor in diabetes. This could contribute to the disturbance of glomerular blood flow and the development of diabetic nephropathy. The aim of this study was to determine whether a similar receptor abnormality occurs in patients with type I insulin-dependent diabetes mellitus (IDDM) and if so whether this is more prevalent in patients with micro- or macro-albuminuria. The platelet AII receptor was chosen because of its availability from the circulation and its comparable regulatory properties to tissue-based receptors. The interaction between plasma AII and its platelet receptor was examined in 45 patients with IDDM and 36 age- and sex-matched control subjects. Seven patients had clinical nephropathy and two had persistent micro-albuminuria. The duration of diabetes varied from 1 month to 42 years. There was a significant inverse correlation between plasma AII and the logarithm of receptor number in the control group (r = -0.555, P < 0.001). This relationship was not observed in the diabetic patients irrespective of the duration of disease or the presence of nephropathy. Receptor expression in patients without nephropathy showed no correlation with either duration of disease or the degree of glycaemic control. However, a significant relationship between AII receptor number and duration of diabetes was noted in the group with nephropathy (r = 0.723, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗