SREBP-1 Proteins

Quinc

Member
In the 2nd part of his article series, Tom Rayhawk examines in detail, different (and well known) nutrients and supplements and their impact on SREBP-1c levels. In particular, Tom discusses the use of CLA (you may be surprised by his findings), Arachodonic Acid and Berberine

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In the 2nd part of his article series, Tom Rayhawk examines in detail, different (and well known) nutrients and supplements and their impact on SREBP-1c levels. In particular, Tom discusses the use of CLA (you may be surprised by his findings), Arachodonic Acid and Berberine

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Pretty interesting, especially when he talks about fructose being the most active in increasing SREBP-1c levels- high fructose cs is in just about everything now- so it does not surprise me- the more research I read about hfcs, the less I want to eat candy (although I do love those gummi raspberries and gummi coke bottles LOL)
 
Am J Clin Nutr. 2004 Apr;79(4):537-43.Click here to read Links

Erratum in:
Am J Clin Nutr. 2004 Oct;80(4):1090.

Comment in:
Am J Clin Nutr. 2004 Nov;80(5):1446-7; author reply 1447-8.
Am J Clin Nutr. 2004 Oct;80(4):1081; author reply 1081-2.

Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.

* Bray GA,
* Nielsen SJ,
* Popkin BM.

Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA. [email protected]

Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.


Obes Res. 2005 Jul;13(7):1146-56.Click here to read Links
Consuming fructose-sweetened beverages increases body adiposity in mice.

* Jurgens H,
* Haass W,
* Castaneda TR,
* Schurmann A,
* Koebnick C,
* Dombrowski F,
* Otto B,
* Nawrocki AR,
* Scherer PE,
* Spranger J,
* Ristow M,
* Joost HG,
* Havel PJ,
* Tschop MH.

Department of Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany. [email protected]

OBJECTIVE: The marked increase in the prevalence of obesity in the United States has recently been attributed to the increased fructose consumption. To determine if and how fructose might promote obesity in an animal model, we measured body composition, energy intake, energy expenditure, substrate oxidation, and several endocrine parameters related to energy homeostasis in mice consuming fructose. RESEARCH METHODS AND PROCEDURES: We compared the effects of ad libitum access to fructose (15% solution in water), sucrose (10%, popular soft drink), and artificial sweetener (0% calories, popular diet soft drink) on adipogenesis and energy metabolism in mice. RESULTS: Exposure to fructose water increased adiposity, whereas increased fat mass after consumption of soft drinks or diet soft drinks did not reach statistical significance (n = 9 each group). Total intake of energy was unaltered, because mice proportionally reduced their caloric intake from chow. There was a trend toward reduced energy expenditure and increased respiratory quotient, albeit not significant, in the fructose group. Furthermore, fructose produced a hepatic lipid accumulation with a characteristic pericentral pattern. DISCUSSION: These data are compatible with the conclusion that a high intake of fructose selectively enhances adipogenesis, possibly through a shift of substrate use to lipogenesis.
Taiwan Yi Xue Hui Za Zhi. 1989 Sep;88(9):883-5. Links
Effects of high-fructose (90%) corn syrup on plasma glucose, insulin, and C-peptide in non-insulin-dependent diabetes mellitus and normal subjects.

* Hung CT.

Interest in sweetening agents is encouraging manufacturers and researchers to find a safe substance to maintain the life quality of diabetics. The popularity of sweetened food items has increased recently in Taiwan. The glycemic index of fructose has been reported to be 20%, much lower than most carbohydrate foods. A high-fructose corn syrup (HFCS) has come onto the market of sweetening agents and has been proposed as a low-cost substitute for fructose in dietetic management of diabetes. The aim of this study was to compare the glycemic effects of HFCS and glucose to see if there is a place for high-fructose corn syrup in diabetic management. In 8 normal and 21 non-insulin dependent diabetes mellitus (NIDDM) subjects, we performed oral tolerance tests. After an overnight fast, the subjects were given either 75g of glucose or an equivalent amount of HFCS containing 75g of carbohydrate. Blood was sampled before and at 30, 60, 90, 120 and 180 minutes after the glucose load. Blood glucose was analyzed by the glucose oxidase method using YSI 23 A (Yellow-Springs Intrument). The insulin and C-peptide were measured by RIA kits from Daiichi. The area under the curves (AUC) was calculated for plasma glucose, immunoreactive insulin (IRI) and immunoreactive C-peptide (IRCP). The results showed that the glycemic effect of HFCS was 73% of glucose. The AUC of IRI after HFCS was 56% of that of glucose. The AUC of IRCP after HFCS was 57% of that of glucose. The high glycemic index of HFCS in our study does not support the use of HFCS as a substitute for fructose.
 
J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72.Click here to read Links
Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.

* Teff KL,
* Elliott SS,
* Tschop M,
* Kieffer TJ,
* Rader D,
* Heiman M,
* Townsend RR,
* Keim NL,
* D'Alessio D,
* Havel PJ.

Monell Chemical Senses Center, University of Pennsylvania, Philadelphia 19104, USA.

Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Because fructose, unlike glucose, does not stimulate insulin secretion, we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose. Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30, and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGl)] beverage. Meals were isocaloric in the two treatments. Postprandial glycemic excursions were reduced by 66 +/- 12%, and insulin responses were 65 +/- 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 +/- 7%; P < 0.005), the entire 24 h (-21 +/- 8%; P < 0.02), and the diurnal amplitude (peak - nadir) (24 +/- 6%; P < 0.0025) were reduced on the HFr day compared with the HGl day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGl meal (P < 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGl). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day (P < 0.005). Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.


Am J Clin Nutr. 2002 Nov;76(5):911-22.Click here to read Links

Comment in:
Am J Clin Nutr. 2003 Oct;78(4):804-5; author reply 805-6.

Fructose, weight gain, and the insulin resistance syndrome.

* Elliott SS,
* Keim NL,
* Stern JS,
* Teff K,
* Havel PJ.

Department of Nutrition, University of California, Davis 95616, USA.

This review explores whether fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome. The per capita disappearance data for fructose from the combined consumption of sucrose and high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic beta cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans.
 
It's not all cut and dry though with fructose, though. As mentioned in part 1 glucose followed by sucrose and THEN fructose were considered when comparing the lipogenic potential of different monosaccharides. However, HFCS is simply a poor food choice period but straigh up fructose and its negative implications relative to its metabolism by the liver and adipose-inducing issues has to be respected.
 
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