Effect of short-term fasting on lipid kinetics in lean and obese women

Horowitz, Jeffrey F.; Coppack, Simon W.; Paramore, Deanna S.; Cryer, Philip E.; Zhao, Guoqing; Klein, Samuel

doi:10.1152/ajpendo.1999.276.2.e278

Cited by 102 publications

(118 citation statements)

References 29 publications

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“…Since insulin is the major regulator of basal adipose tissue lipolytic activity (19,20), the higher rates of nocturnal and postprandial lipolysis in our diabetic subjects compared with control subjects were due at least in part to resistance to the antilipolytic effects of insulin in adipose tissue. In fact, the diabetic subjects had higher lipolytic rates in spite of threefold greater plasma insulin concentrations compared with control subjects.…”

Section: Discussionmentioning

confidence: 87%

Nocturnal and Postprandial Free Fatty Acid Kinetics in Normal and Type 2 Diabetic Subjects

et al. 2003

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Whether free fatty acid (FFA) rate of appearance (R a ) is increased in type 2 diabetes is controversial. To characterize nocturnal and postprandial abnormalities in FFA kinetics and to determine the effects of treatment with insulin sensitizers on lipolysis, we measured palmitate R a in control subjects (n ‫؍‬ 6) and individuals with poorly controlled, sulfonylurea-treated type 2 diabetes (HbA 1c ‫؍‬ 8.7 ؎ 0.2%, n ‫؍‬ 20), the latter before and at the end of 12 weeks of treatment with troglitazone (600 mg/day, n ‫؍‬ 4), metformin (ϳ2,000 mg/day, n ‫؍‬ 8), or placebo (n ‫؍‬ 8). Subjects consumed a standard breakfast at 0800 h. Results in control subjects and type 2 diabetic subjects were compared at baseline. Integrated nocturnal FFA R a (AUC 1:00 -8:00 A.M. ) was ϳ50% higher in type 2 diabetic subjects than in control subjects (29.4 ؎ 3.0 vs. 19.4 ؎ 3.9 mmol ⅐ m ؊2 ⅐ 7 h ؊1 , respectively, P < 0.05), whereas postprandial palmitate R a (AUC 0 -240 min ) was almost threefold higher in type 2 diabetic subjects than in control subjects (14.2 ؎ 1.7 vs. 5.3 ؎ 1.0 mmol ⅐ m ؊2 ⅐ 4 h ؊1 , respectively, P < 0.01). After troglitazone treatment, nocturnal palmitate R a did not change, but postprandial palmitate R a decreased by ϳ30% (P < 0.05). Palmitate kinetics did not change with metformin or placebo treatment. In summary, nocturnal and postprandial FFA R a is increased in type 2 diabetes. Postprandial lipolysis appears to be preferentially improved by thiazolidinediones compared with nocturnal lipolysis. Diabetes 52:675-681, 2003 P atients with type 2 diabetes have resistance to the antilipolytic effects of insulin on adipose tissue (1,2). This dysregulation of adipose tissue lipolysis has been implicated as a major cause of the abnormalities in lipoprotein and glucose metabolism that are characteristic of type 2 diabetes (3). However, plasma free fatty acid (FFA) turnover has been reported to be both increased (4) and normal (5-8) in type 2 diabetes.FFA tracer studies in patients with type 2 diabetes have generally been performed under postabsorptive conditions (4,5,7) or during a hyperinsulinemic-euglycemic clamp (1,2); little information is available regarding nocturnal and postprandial FFA metabolism. In fact, patients with poorly controlled type 2 diabetes exhibit an increase in plasma FFA concentrations during the night (9), but it is not known whether this is the result of increased release of FFA into the systemic circulation or decreased plasma FFA clearance. An understanding of fatty acid metabolism during nocturnal and absorptive conditions is important because postabsorptive measurements may not necessarily reflect conditions at other times of the day.The treatment of type 2 diabetes has been revolutionized by the availability of medications, including biguanides and thiazolidinediones, which improve insulin action on glucose metabolism. In addition, some (10,11) but not all (12) studies suggest that these agents may improve abnormalities in FFA metabolism in the postabsorptive state and during hyperinsulin...

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Section: Discussionmentioning

confidence: 87%

Nocturnal and Postprandial Free Fatty Acid Kinetics in Normal and Type 2 Diabetic Subjects

et al. 2003

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“…10,11,29,37 In the absence of any significant increase in GH secretion obese patients in our study showed normal activation of lipolysis; this probably reflects the fasting-induced response of other contraregulatory hormones. 38 In this context, modification in IGF-I bioactivity brought about by fasting-induced changes in the most important binding proteins could play a major metabolic role. 39,40 In conclusion, short-term fasting does not stimulate mean GH concentration in obesity as well as in hypopituitary patients with severe GHD.…”

Section: Discussionmentioning

confidence: 99%

Effects of 36 hour fasting on GH/IGF-I axis and metabolic parameters in patients with simple obesity. Comparison with normal subjects and hypopituitary patients with severe GH deficiency

et al. 2001

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OBJECTIVE: Reduction of growth hormone (GH) secretion in obesity probably reflects neuroendocrine and metabolic abnormalities. Even short-term fasting stimulates GH secretion and distinguishes normal from hypopituitary subjects with growth hormone deficiency (GHD). Marked weight loss improves GH secretion in obesity but the effect of fasting is controversial. We studied the effects of a 36 h fasting on the GH=IGF-I axis and metabolic parameters in obesity. SUBJECTS: We studied nine obese patients (OB; three male and six female; age, 29.2 AE 4.8; range, 18 -59 y; body mass index (BMI), 43.4 AE 2.7 kg=m 2 ; WHR, 0.9 AE 0.1). Fifteen normal subjects (NS; eight male and seven female 28.9 AE 0.6, 25 -35 y; 21.6 AE 0.4 kg=m 2 ) and 10 adult hypopituitary patients with severe GH deficiency (GHD; seven male and three female; 37.6 AE 2.3, 29 -50 y; 24.5 AE 1.0 kg=m 2 ; GH peak < 3mg=l after ITT and=or < 9mg=l after GHRH þ arginine) served as control groups. STUDY DESIGN: We studied the effects of 36 h fasting on 8 h diurnal mean GH, insulin and glucose concentrations (mGHc, mINSc and mGLUc; assay every 30 min from 8.00 am to 4.00 pm) as well as on IGF-I, IGFBP-3, ALS, IGFBP-1, GHBP and free fatty acid (FFA) levels. RESULTS: Before fasting, basal IGF-I and ALS levels in OB were similar to those in NS and both were higher (P < 0.001) than those in GHD. IGFBP-3 levels in OB were lower (P < 0.01) than in NS but higher (P < 0.02) than in GHD. GHBP levels in OB and GHD were similar and both were higher (P < 0.01) than in NS. Glucose levels were similar in all groups. FFA levels in OB were higher (P < 0.01) than in NS but similar to those in GHD. IGFBP-1 in OB were lower (P < 0.05) than in NS and GHD which, in turn, were similar. On the other hand, mINSc in OB was higher (P < 0.01) than that in NS and GHD which, in turn, were similar. The mGHc in OB was similar to that in NS but only the latter was higher (P < 0.05) than in GHD. The individual mGHc in the three groups overlapped. After fasting, IGF-I levels in GHD were unchanged while they decreased in OB (P ¼ NS) as well as in NS (P < 0.01). IGFBP-3 and ALS levels did not change. GHBP levels in OB and GHD were unchanged while they increased in NS (P < 0.01). Glucose and FFA levels were reduced and increased, respectively, in all groups (P < 0.02 and P < 0.01). IGFBP-1 increased while mINSc decreased in all groups (P < 0.02 and P < 0.01); in OB they persisted lower and higher (P < 0.01) respectively, than in NS and GHD. Fasting significantly increased mGHc in NS (P < 0.001) but not in OB as well as in GHD. Individual mGHc in OB showed persistent overlap with GHD. CONCLUSIONS: Short-term fasting does not increase GH secretion in obesity and does not distinguish somatotroph function in obese from that in severe GHD adults. Short-term fasting in obesity has attenuated effects on insulin and IGFBP-1 secretion while it normally increases free fatty acids in spite of any change in GH secretion.

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“…Local noradrenaline spillover from a subcutaneous adipose tissue bed does not change significantly between the overnight fasted state (14 h fast) and 22 h fast. 81 In contrast, there is increased noradrenaline spillover from adipose tissue associated with (and possibly causing) increased local blood flow 60-120 min after eating and after 72 h fasting. 64,82 In addition to acute effects on adipose tissue function, the SNS innervation appears to affect cell numbers.…”

Section: Innervation Of White Adipose Tissuementioning

confidence: 99%

Integrative physiology of human adipose tissue

et al. 2003

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Adipose tissue is now recognised as a highly active metabolic and endocrine organ. Great strides have been made in uncovering the multiple functions of the adipocyte in cellular and molecular detail, but it is essential to remember that adipose tissue normally operates as a structured whole. Its functions are regulated by multiple external influences such as autonomic nervous system activity, the rate of blood flow and the delivery of a complex mix of substrates and hormones in the plasma. Attempting to understand how all these factors converge and regulate adipose tissue function is a prime example of integrative physiology. Adipose tissue metabolism is extremely dynamic, and the supply of and removal of substrates in the blood is acutely regulated according to the nutritional state. Adipose tissue possesses the ability to a very large extent to modulate its own metabolic activities, including differentiation of new adipocytes and production of blood vessels as necessary to accommodate increasing fat stores. At the same time, adipocytes signal to other tissues to regulate their energy metabolism in accordance with the body's nutritional state. Ultimately adipocyte fat stores have to match the body's overall surplus or deficit of energy. This implies the existence of one (or more) signal(s) to the adipose tissue that reflects the body's energy status, and points once again to the need for an integrative view of adipose tissue function.

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Effect of short-term fasting on lipid kinetics in lean and obese women

Cited by 102 publications

References 29 publications

Nocturnal and Postprandial Free Fatty Acid Kinetics in Normal and Type 2 Diabetic Subjects

Nocturnal and Postprandial Free Fatty Acid Kinetics in Normal and Type 2 Diabetic Subjects

Effects of 36 hour fasting on GH/IGF-I axis and metabolic parameters in patients with simple obesity. Comparison with normal subjects and hypopituitary patients with severe GH deficiency

Integrative physiology of human adipose tissue

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